psychgirl
TB Fanatic
It’s quite an astounding library of historical record, isn’t it??
She’s a total warrior!
CORONA Main Coronavirus thread
- Thread starter Heliobas Disciple
- Start date
-
- Tags
- coronavirus
She’s a total warrior!
herbgarden
Veteran Member
I thank you ,also, for all the work you put in to keep us informed.
Heliobas Disciple
TB Fanatic
Thank you for your kind words, and for the agreements and likes to all of them. I agree, that (unfortunately) the subject is still important ... I wish it wasn't... but as long as it is, I'll keep trying to keep us all informed.
HD
Heliobas Disciple
TB Fanatic
(fair use applies)
Emerging SARS-CoV-2 Variant RE.1.1 On Track to Dominate and Spark New COVID-19 Surges
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 01, 2026
As the world continues to grapple with evolving SARS-CoV-2 strains, a new variant designated RE.1.1—descended from the BA.3.2 lineage—is emerging as a potential driver of increased infections. First identified in sequences from Australia, RE.1.1 features recombinant elements, including segments from JF.1 in the M, ORF6, and partial ORF7a genes. This hypermutated profile, sometimes nicknamed part of the "Cicada" family under BA.3.2, raises concerns about enhanced transmissibility and immune evasion. In the broader landscape of world Medical News, organizations like the WHO have highlighted rising COVID-19 activity across regions, with various new variants including new lineages form the BA.3.2 strains, fueling surges in Southeast Asia, Europe, and North America.
While NB.1.8.1 has dominated past headlines for its rapid spread and links to higher viral loads, RE.1.1 appears positioned to follow suit, potentially outcompeting predecessors due to antigenic drift that boosts effective reproduction numbers (Re).
Experts warn that without updated surveillance, this could mirror past waves, with breakthroughs in vaccinated populations.
Origins and Genetic Profile
RE.1.1 alias BA.3.2.2.1.1, traces its origins with recombination breakpoints identified between nucleotides 26275-26529 and 27384-27597.
This genetic shuffling, observed in samples like EPI_ISL_20275963 from New South Wales, Australia, incorporates mutations that may enhance replication speed and evade T-cell epitopes.
Unlike earlier strains, RE.1.1's brute-force infection mechanism could lead to prolonged shedding in immunocompromised individuals, amplifying community transmission.
Projected Impact Globally
In countries where tourism and dense urban centers heighten vulnerability, RE.1.1 could exploit existing immunity gaps, potentially causing a late Winter and early Spring wave.
European data shows another close sub-lineage RE.2's fast initial growth, contrasting slower RE.1 uptake in Australia and suggesting immune landscapes play a role.
Globally, this variant's rise might overwhelm healthcare systems, echoing severity tied to certain HLA types.
Recommendations for Mitigation
Health authorities should start advocating masking and urgent deployment of clean-air strategies in schools, offices, malls and in all crowded and public places. Ongoing genomic sequencing is crucial to track RE.1.1's trajectory.
As RE.1.1 edges toward predominance, proactive measures could avert a major surge, but delays risk repeating history's costly lessons.
Emerging SARS-CoV-2 Variant RE.1.1 On Track to Dominate and Spark New COVID-19 Surges
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 01, 2026
As the world continues to grapple with evolving SARS-CoV-2 strains, a new variant designated RE.1.1—descended from the BA.3.2 lineage—is emerging as a potential driver of increased infections. First identified in sequences from Australia, RE.1.1 features recombinant elements, including segments from JF.1 in the M, ORF6, and partial ORF7a genes. This hypermutated profile, sometimes nicknamed part of the "Cicada" family under BA.3.2, raises concerns about enhanced transmissibility and immune evasion. In the broader landscape of world Medical News, organizations like the WHO have highlighted rising COVID-19 activity across regions, with various new variants including new lineages form the BA.3.2 strains, fueling surges in Southeast Asia, Europe, and North America.
While NB.1.8.1 has dominated past headlines for its rapid spread and links to higher viral loads, RE.1.1 appears positioned to follow suit, potentially outcompeting predecessors due to antigenic drift that boosts effective reproduction numbers (Re).
Experts warn that without updated surveillance, this could mirror past waves, with breakthroughs in vaccinated populations.
Origins and Genetic Profile
RE.1.1 alias BA.3.2.2.1.1, traces its origins with recombination breakpoints identified between nucleotides 26275-26529 and 27384-27597.
This genetic shuffling, observed in samples like EPI_ISL_20275963 from New South Wales, Australia, incorporates mutations that may enhance replication speed and evade T-cell epitopes.
Unlike earlier strains, RE.1.1's brute-force infection mechanism could lead to prolonged shedding in immunocompromised individuals, amplifying community transmission.
Projected Impact Globally
In countries where tourism and dense urban centers heighten vulnerability, RE.1.1 could exploit existing immunity gaps, potentially causing a late Winter and early Spring wave.
European data shows another close sub-lineage RE.2's fast initial growth, contrasting slower RE.1 uptake in Australia and suggesting immune landscapes play a role.
Globally, this variant's rise might overwhelm healthcare systems, echoing severity tied to certain HLA types.
Recommendations for Mitigation
Health authorities should start advocating masking and urgent deployment of clean-air strategies in schools, offices, malls and in all crowded and public places. Ongoing genomic sequencing is crucial to track RE.1.1's trajectory.
As RE.1.1 edges toward predominance, proactive measures could avert a major surge, but delays risk repeating history's costly lessons.
Tristan
TB Fanatic
Heliobas Disciple
TB Fanatic
(fair use applies)
American Researchers Warn That COVID-19 Womb Exposure is Giving Rise to a New Generation with Brain and Behavior Changes
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 02, 2026
Medical News: A generation shaped before birth
Scientists are increasingly worried that the COVID-19 pandemic may have left invisible marks on babies who were still in the womb when their mothers were infected. A new large and carefully conducted study has now revealed that exposure to the SARS-CoV-2 virus during pregnancy may subtly but meaningfully change how a baby’s brain develops and how the child thinks and behaves later in life. This Medical News report highlights findings that are especially important for parents, teachers and healthcare workers to understand.
Who conducted the research
The study was carried out by researchers from the Developing Brain Institute at Children’s National Hospital in Washington DC. Several authors were also affiliated with the Department of Pediatrics and the Department of Obstetrics and Gynecology at George Washington University School of Medicine and Health Sciences. The research team included experts in pediatric neurology, psychology, brain imaging and child development.
How the study was done
The scientists followed 142 mother baby pairs. Of these 39 babies were exposed to COVID-19 during pregnancy while 103 babies were born before the pandemic and served as a comparison group. When the babies were about two weeks old, they underwent safe non-invasive MRI brain scans while asleep. At around two years of age trained specialists assessed the children using well established developmental and behavioral tests.
What changed in newborn brains
The brain scans showed clear differences in babies exposed to COVID-19 in the womb. Some brain areas such as the outer gray matter and the left hippocampus were larger than normal while other regions including deeper gray matter and white matter were smaller. These areas are crucial for memory learning emotional control and communication. The changes were not random but followed a pattern seen in other conditions involving early brain stress or inflammation.
Effects seen at two years of age
When the children reached toddler age, those exposed to COVID-19 during pregnancy scored lower on thinking and problem-solving tests. More than half of them were considered at risk for developmental delay compared to only a small fraction of children born before the pandemic. Parents also reported more signs of anxiety withdrawal and emotional sensitivity. Importantly language understanding was affected even when overall speech seemed normal.
Why these changes may happen
The researchers believe the virus itself rarely reaches the baby. Instead, the mother’s immune response may release inflammatory signals that affect the developing brain. Changes in the placenta oxygen supply and even gene regulation may also play a role. The study showed that early brain structure changes hel ped explain later thinking and emotional difficulties.
What this means for families and society
These findings do not mean that every COVID-19 exposed child will struggle. Many children will develop normally. However, the results suggest that this group may benefit from closer developmental monitoring and early support. Identifying issues early can greatly improve long-term outcomes.
Conclusion
This important study shows that COVID-19 exposure during pregnancy is linked to measurable brain changes at birth and lower cognitive and emotional scores by age two. The findings emphasize that the pandemic’s impact extends beyond immediate infection and may shape early childhood development. Ongoing follow up early screening and timely interventions could help reduce long term risks for this COVID-19 generation.
The study findings were published in the peer reviewed journal: Brain Behavior and Immunity.
American Researchers Warn That COVID-19 Womb Exposure is Giving Rise to a New Generation with Brain and Behavior Changes
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 02, 2026
Medical News: A generation shaped before birth
Scientists are increasingly worried that the COVID-19 pandemic may have left invisible marks on babies who were still in the womb when their mothers were infected. A new large and carefully conducted study has now revealed that exposure to the SARS-CoV-2 virus during pregnancy may subtly but meaningfully change how a baby’s brain develops and how the child thinks and behaves later in life. This Medical News report highlights findings that are especially important for parents, teachers and healthcare workers to understand.
Who conducted the research
The study was carried out by researchers from the Developing Brain Institute at Children’s National Hospital in Washington DC. Several authors were also affiliated with the Department of Pediatrics and the Department of Obstetrics and Gynecology at George Washington University School of Medicine and Health Sciences. The research team included experts in pediatric neurology, psychology, brain imaging and child development.
How the study was done
The scientists followed 142 mother baby pairs. Of these 39 babies were exposed to COVID-19 during pregnancy while 103 babies were born before the pandemic and served as a comparison group. When the babies were about two weeks old, they underwent safe non-invasive MRI brain scans while asleep. At around two years of age trained specialists assessed the children using well established developmental and behavioral tests.
What changed in newborn brains
The brain scans showed clear differences in babies exposed to COVID-19 in the womb. Some brain areas such as the outer gray matter and the left hippocampus were larger than normal while other regions including deeper gray matter and white matter were smaller. These areas are crucial for memory learning emotional control and communication. The changes were not random but followed a pattern seen in other conditions involving early brain stress or inflammation.
Effects seen at two years of age
When the children reached toddler age, those exposed to COVID-19 during pregnancy scored lower on thinking and problem-solving tests. More than half of them were considered at risk for developmental delay compared to only a small fraction of children born before the pandemic. Parents also reported more signs of anxiety withdrawal and emotional sensitivity. Importantly language understanding was affected even when overall speech seemed normal.
Why these changes may happen
The researchers believe the virus itself rarely reaches the baby. Instead, the mother’s immune response may release inflammatory signals that affect the developing brain. Changes in the placenta oxygen supply and even gene regulation may also play a role. The study showed that early brain structure changes hel ped explain later thinking and emotional difficulties.
What this means for families and society
These findings do not mean that every COVID-19 exposed child will struggle. Many children will develop normally. However, the results suggest that this group may benefit from closer developmental monitoring and early support. Identifying issues early can greatly improve long-term outcomes.
Conclusion
This important study shows that COVID-19 exposure during pregnancy is linked to measurable brain changes at birth and lower cognitive and emotional scores by age two. The findings emphasize that the pandemic’s impact extends beyond immediate infection and may shape early childhood development. Ongoing follow up early screening and timely interventions could help reduce long term risks for this COVID-19 generation.
The study findings were published in the peer reviewed journal: Brain Behavior and Immunity.
Heliobas Disciple
TB Fanatic
(fair use applies)
Researchers Warn That COVID-19 Infections Are Quietly Rewiring the Human Brain on a Molecular Level
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 04, 2026
A new scientific study has revealed troubling evidence that COVID-19 infection is leaving lasting changes in the human brain, potentially explaining why many survivors experience lingering memory problems, mood disorders, anxiety, and other neurological symptoms long after recovery.
Researchers analyzed brain tissue at an unprecedented level of detail, focusing on how COVID-19 alters the way brain cells process genetic instructions. Their findings suggest that the virus may disrupt essential communication systems inside brain cells, especially neurons responsible for thinking, memory, and emotional control.
This Medical News report highlights research conducted by scientists from the Institute for Clinical Medical Research at The First Affiliated Hospital of Xiamen University, the Xiamen Cell Therapy Research Center, and the Department of Pulmonary and Critical Care Medicine at The First Affiliated Hospital of Xiamen University in China.
Looking Deep Inside Brain Cells
The research team studied frontal cortex brain samples from people who died with COVID-19 and compared them to non-infected individuals. Using advanced single cell analysis, they examined how brain cells modify messenger RNA, a crucial molecule that tells cells how to make proteins.
One key process they studied is called alternative polyadenylation. While the name sounds complex, it simply refers to how cells decide where to end a genetic message. This decision affects how stable the message is, how much protein is produced, and how long the message lasts. Small changes in this process can have big effects on brain health.
Neurons Show the Most Damage
The study found that neurons were especially affected after COVID-19 infection. In healthy brains, neurons usually produce longer genetic messages that support stable communication and learning. After infection, many neurons shifted toward producing shorter and less stable messages.
This shift was strongly linked to genes involved in memory formation, learning ability, synaptic signaling, and overall brain development. Researchers observed that important brain support genes such as NEFL, APP, and CALM1 showed disrupted processing, which may weaken nerve fibers and reduce communication between brain cells.
Links to Mental and Neurological Disorders
One of the most alarming findings was the identification of 267 genes linked to known neurological and psychiatric disorders that were altered after COVID-19 infection. These genes are associated with conditions such as Alzheimer disease, Parkinson disease, schizophrenia, depression, anxiety, epilepsy, and cognitive decline.
The study also revealed that many of these genetic changes interfere with microRNA regulation, a system that normally keeps brain activity balanced. When this regulation is disturbed, brain ce lls may overreact to stress or inflammation, increasing the risk of long-term mental health problems.
Why This Matters
These findings provide strong biological evidence that COVID-19 is not just a respiratory illness but can quietly reprogram the brain at a molecular level. The changes observed do not necessarily mean immediate brain damage, but they may increase vulnerability to neurological and psychiatric disorders months or even years later.
Conclusion
The study strongly suggests that COVID-19 infection triggers subtle yet widespread genetic changes in brain cells that affect how neurons function, communicate, and survive. By disrupting key pathways related to memory, cognition, and emotional regulation, these molecular shifts may explain the persistent brain fog, mood disorders, and neurological symptoms reported by many COVID survivors. Understanding these hidden changes opens the door to better diagnosis, monitoring, and future treatments aimed at protecting long term brain health.
The study findings were published in the peer reviewed journal: PLOS One
journals.plos.org
Researchers Warn That COVID-19 Infections Are Quietly Rewiring the Human Brain on a Molecular Level
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 04, 2026
A new scientific study has revealed troubling evidence that COVID-19 infection is leaving lasting changes in the human brain, potentially explaining why many survivors experience lingering memory problems, mood disorders, anxiety, and other neurological symptoms long after recovery.
Researchers analyzed brain tissue at an unprecedented level of detail, focusing on how COVID-19 alters the way brain cells process genetic instructions. Their findings suggest that the virus may disrupt essential communication systems inside brain cells, especially neurons responsible for thinking, memory, and emotional control.
This Medical News report highlights research conducted by scientists from the Institute for Clinical Medical Research at The First Affiliated Hospital of Xiamen University, the Xiamen Cell Therapy Research Center, and the Department of Pulmonary and Critical Care Medicine at The First Affiliated Hospital of Xiamen University in China.
Looking Deep Inside Brain Cells
The research team studied frontal cortex brain samples from people who died with COVID-19 and compared them to non-infected individuals. Using advanced single cell analysis, they examined how brain cells modify messenger RNA, a crucial molecule that tells cells how to make proteins.
One key process they studied is called alternative polyadenylation. While the name sounds complex, it simply refers to how cells decide where to end a genetic message. This decision affects how stable the message is, how much protein is produced, and how long the message lasts. Small changes in this process can have big effects on brain health.
Neurons Show the Most Damage
The study found that neurons were especially affected after COVID-19 infection. In healthy brains, neurons usually produce longer genetic messages that support stable communication and learning. After infection, many neurons shifted toward producing shorter and less stable messages.
This shift was strongly linked to genes involved in memory formation, learning ability, synaptic signaling, and overall brain development. Researchers observed that important brain support genes such as NEFL, APP, and CALM1 showed disrupted processing, which may weaken nerve fibers and reduce communication between brain cells.
Links to Mental and Neurological Disorders
One of the most alarming findings was the identification of 267 genes linked to known neurological and psychiatric disorders that were altered after COVID-19 infection. These genes are associated with conditions such as Alzheimer disease, Parkinson disease, schizophrenia, depression, anxiety, epilepsy, and cognitive decline.
The study also revealed that many of these genetic changes interfere with microRNA regulation, a system that normally keeps brain activity balanced. When this regulation is disturbed, brain ce lls may overreact to stress or inflammation, increasing the risk of long-term mental health problems.
Why This Matters
These findings provide strong biological evidence that COVID-19 is not just a respiratory illness but can quietly reprogram the brain at a molecular level. The changes observed do not necessarily mean immediate brain damage, but they may increase vulnerability to neurological and psychiatric disorders months or even years later.
Conclusion
The study strongly suggests that COVID-19 infection triggers subtle yet widespread genetic changes in brain cells that affect how neurons function, communicate, and survive. By disrupting key pathways related to memory, cognition, and emotional regulation, these molecular shifts may explain the persistent brain fog, mood disorders, and neurological symptoms reported by many COVID survivors. Understanding these hidden changes opens the door to better diagnosis, monitoring, and future treatments aimed at protecting long term brain health.
The study findings were published in the peer reviewed journal: PLOS One
Single-cell alternative polyadenylation analysis reveals mechanistic insights of COVID-19-associated neurological and psychiatric effects
COVID-19 is associated with increased risks of neurological and psychiatric sequelae. Alternative polyadenylation (APA) is ubiquitous in human genes, resulting in mRNA diversity, and has been validated to play a pivotal regulatory role in the onset and progression of a variety of diseases...
journals.plos.org
Heliobas Disciple
TB Fanatic
Your Body's Dangerous Adaptation to COVID
Vejon Health
Streamed live January 5, 2025
23 min 1 sec
Discover how the immune system responds to COVID-19—and how that response may be changing over time. In this video, we explore the complex immune processes that are activated when the body encounters the virus, from early recognition to antibody and cellular responses. But we also examine an important and often overlooked question: what happens when the immune system becomes quieter, more tolerant, or less reactive with repeated exposure?
========================================================
Selva, Kevin J., et al. "Elevated SARS-CoV-2 IgG4 in plasma and mucosa following repeated mRNA boosters impact antibody functions to Omicron and sarbecoviruses." EBioMedicine 123 (2026): 106087.
========================================================
By understanding not just how immunity fights infection, but how it adapts, dampens inflammation, and sometimes prioritises tolerance over clearance, we gain deeper insight into reinfection risk, immune efficiency, and long-term health. This discussion goes beyond simple protection narratives and looks at how vaccination, prior infection, and immune regulation shape our ongoing relationship with COVID-19. Watch to better understand your immune system—and why a reduced response isn’t always the same as a resolved problem.
Heliobas Disciple
TB Fanatic
(fair use applies)
The Shocking Speed at Which Pandemics Take Over Cities
By Columbia University's Mailman School of Public Health
January 5, 2026
Both H1N1 and COVID-19 spread across the U.S. faster and more unpredictably than early detection systems could keep up.
Public health scientists at the Columbia University Mailman School of Public Health used advanced computer simulations to retrace how the 2009 H1N1 flu pandemic and the 2020 COVID-19 pandemic spread across the United States. Their analysis shows just how quickly respiratory pandemics can move and why stopping outbreaks early is so difficult. Published today (January 5) in the journal Proceedings of the National Academy of Sciences, the research is the first study to directly compare how these two major U.S. pandemics spread across metropolitan areas nationwide.
A Look Back at Two Major U.S. Pandemics
The impact of both outbreaks was severe. In the United States, the 2009 H1N1 flu pandemic led to 274,304 hospitalizations and 12,469 deaths. The COVID-19 pandemic has had an even greater toll, with 1.2 million confirmed deaths so far.
The research team set out to better understand how these pandemics traveled from place to place in order to improve preparedness for future outbreaks. To do this, they combined detailed information about how each disease spreads with computer models that incorporated air travel, daily commuting patterns, and the possibility of superspreading events. Their simulations covered more than three hundred metropolitan areas across the U.S.
Rapid Spread Before Detection
The results showed that both pandemics were already circulating widely in most major metro areas within just a few weeks. This rapid expansion often happened before early case detection or government response measures were in place. Although the exact routes of transmission differed between H1N1 and COVID-19, both relied on key urban hubs to fuel nationwide spread. Cities such as New York and Atlanta played major roles. Air travel emerged as the dominant factor driving spread, far more than commuting, but unpredictable transmission patterns made it extremely difficult to forecast where outbreaks would surge next.
“The rapid and uncertain spread of the 2009 H1N1 flu and 2020 COVID-19 pandemics underscores the challenges for timely detection and control. Expanding wastewater surveillance coverage coupled with effective infection control could potentially slow the initial spread of future pandemics,” says the study’s senior author, Sen Pei, PhD, assistant professor of environmental health sciences at Columbia Mailman School.
Previous research has already highlighted the value of wastewater surveillance programs for detecting outbreaks early. This new study adds further support, showing that broader wastewater monitoring could play a key role in strengthening pandemic preparedness and improving response times.
Lessons for Future Outbreaks
In addition to reconstructing how H1N1 and COVID-19 spread, the study introduces a flexible framework that can be used to study the early stages of other epidemics. While human movement, especially air travel, is a major driver of pandemic spread, the researchers emphasize that many other factors also influence outcomes. These include population demographics, school calendars, holiday travel, and weather conditions.
Research Team and Ongoing Work
The study’s first author is Renquan Zhang, Dalian University of Technology, Dalian, China. Additional contributors include Rui Deng and Sitong Liu from Dalian University of Technology; Qing Yao and Jeffrey Shaman from Columbia University; Bryan T. Grenfell from Princeton; and Cécile Viboud from the National Institutes of Health.
For more than ten years, Jeffrey Shaman and colleagues, including Sen Pei, have worked on improving methods to track and predict the spread of infectious diseases such as influenza and COVID-19. Their real-time forecasting tools estimate how fast outbreaks will grow, where they are likely to spread, and when they may peak, helping public health officials make more informed decisions.
Reference: “Reconstructing the early spatial spread of pandemic respiratory viruses in the United States” 5 January 2026, Proceedings of the National Academy of Sciences.
DOI: 10.1073/pnas.2518051123
This study was supported by funding from the National Natural Science Foundation of China (12371516), U.S. National Science Foundation (DMS-2229605), the Centers for Disease Control and Prevention (U01CK000592, 75D30122C14289), National Institute of Allergy and Infectious Diseases (R01AI163023), Princeton Catalysis Initiative, Princeton Precision Health, and High Meadows Environmental Institute. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the U.S. National Institutes of Health, Centers for Disease Control and Prevention, or Department of Health and Human Services.
Shaman and Columbia University disclose partial ownership of SK Analytics. Other authors declare no competing interests.
The Shocking Speed at Which Pandemics Take Over Cities
By Columbia University's Mailman School of Public Health
January 5, 2026
Both H1N1 and COVID-19 spread across the U.S. faster and more unpredictably than early detection systems could keep up.
Public health scientists at the Columbia University Mailman School of Public Health used advanced computer simulations to retrace how the 2009 H1N1 flu pandemic and the 2020 COVID-19 pandemic spread across the United States. Their analysis shows just how quickly respiratory pandemics can move and why stopping outbreaks early is so difficult. Published today (January 5) in the journal Proceedings of the National Academy of Sciences, the research is the first study to directly compare how these two major U.S. pandemics spread across metropolitan areas nationwide.
A Look Back at Two Major U.S. Pandemics
The impact of both outbreaks was severe. In the United States, the 2009 H1N1 flu pandemic led to 274,304 hospitalizations and 12,469 deaths. The COVID-19 pandemic has had an even greater toll, with 1.2 million confirmed deaths so far.
The research team set out to better understand how these pandemics traveled from place to place in order to improve preparedness for future outbreaks. To do this, they combined detailed information about how each disease spreads with computer models that incorporated air travel, daily commuting patterns, and the possibility of superspreading events. Their simulations covered more than three hundred metropolitan areas across the U.S.
Rapid Spread Before Detection
The results showed that both pandemics were already circulating widely in most major metro areas within just a few weeks. This rapid expansion often happened before early case detection or government response measures were in place. Although the exact routes of transmission differed between H1N1 and COVID-19, both relied on key urban hubs to fuel nationwide spread. Cities such as New York and Atlanta played major roles. Air travel emerged as the dominant factor driving spread, far more than commuting, but unpredictable transmission patterns made it extremely difficult to forecast where outbreaks would surge next.
“The rapid and uncertain spread of the 2009 H1N1 flu and 2020 COVID-19 pandemics underscores the challenges for timely detection and control. Expanding wastewater surveillance coverage coupled with effective infection control could potentially slow the initial spread of future pandemics,” says the study’s senior author, Sen Pei, PhD, assistant professor of environmental health sciences at Columbia Mailman School.
Previous research has already highlighted the value of wastewater surveillance programs for detecting outbreaks early. This new study adds further support, showing that broader wastewater monitoring could play a key role in strengthening pandemic preparedness and improving response times.
Lessons for Future Outbreaks
In addition to reconstructing how H1N1 and COVID-19 spread, the study introduces a flexible framework that can be used to study the early stages of other epidemics. While human movement, especially air travel, is a major driver of pandemic spread, the researchers emphasize that many other factors also influence outcomes. These include population demographics, school calendars, holiday travel, and weather conditions.
Research Team and Ongoing Work
The study’s first author is Renquan Zhang, Dalian University of Technology, Dalian, China. Additional contributors include Rui Deng and Sitong Liu from Dalian University of Technology; Qing Yao and Jeffrey Shaman from Columbia University; Bryan T. Grenfell from Princeton; and Cécile Viboud from the National Institutes of Health.
For more than ten years, Jeffrey Shaman and colleagues, including Sen Pei, have worked on improving methods to track and predict the spread of infectious diseases such as influenza and COVID-19. Their real-time forecasting tools estimate how fast outbreaks will grow, where they are likely to spread, and when they may peak, helping public health officials make more informed decisions.
Reference: “Reconstructing the early spatial spread of pandemic respiratory viruses in the United States” 5 January 2026, Proceedings of the National Academy of Sciences.
DOI: 10.1073/pnas.2518051123
This study was supported by funding from the National Natural Science Foundation of China (12371516), U.S. National Science Foundation (DMS-2229605), the Centers for Disease Control and Prevention (U01CK000592, 75D30122C14289), National Institute of Allergy and Infectious Diseases (R01AI163023), Princeton Catalysis Initiative, Princeton Precision Health, and High Meadows Environmental Institute. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the U.S. National Institutes of Health, Centers for Disease Control and Prevention, or Department of Health and Human Services.
Shaman and Columbia University disclose partial ownership of SK Analytics. Other authors declare no competing interests.
meandk0610
Veteran Member
This would apply to the vaccine as well due to the mother's immune response.
Heliobas Disciple
TB Fanatic
(fair use applies)
COVID-19 Brain Fog Mystery Finally Explained
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 06, 2026
Medical News: Lingering Mental Effects After COVID-19 Raise New Alarms
Many people who have recovered from COVID-19 continue to complain about memory lapses, poor concentration, confusion, and what is commonly called “brain fog.” A major new scientific review now explains why these problems happen and why they can last for months or even years after infection. This Medical News report is based on an extensive analysis of existing research that examined how COVID-19 affects the blood-brain barrier and immune system over time.
The study was conducted by researchers from the Department of Clinical and Health Psychology, Universitat Autònoma de Barcelona, Spain, the Institut de Recerca Sant Joan de Déu, Spain, Universidad San Sebastián, Chile, CIBERSAM Biomedical Network Research Center of Mental Health, Spain, and the University of Vic–Central University of Catalonia, Spain.
How COVID-19 Triggers Brain Problems
The researchers found that COVID-19 does not need to directly infect the brain to cause cognitive issues. Instead, the virus triggers a powerful immune reaction in the body. This leads to high levels of inflammatory substances called cytokines circulating in the blood. These cytokines can weaken the blood–brain barrier, a protective layer that normally shields the brain from harmful substances.
Once this barrier is compromised, inflammatory signals can enter the brain, activating brain support cells and disrupting normal communication between nerve cells. This helps explain why many patients experience attention problems, memory loss, and slower thinking even after their lungs have healed.
Brain Fog Changes Over Time
The review showed that cognitive symptoms evolve in stages. During the first few weeks of infection, problems mainly affect attention, working memory, and decision-making. These early issues are usually linked to inflammation, low oxygen levels, and overall illness stress rather than permanent brain damage.
Between one and three months after infection, many patients still struggle with concentration and mental fatigue. By six months and beyond, a significant number develop broader cognitive difficulties involving multiple brain functions. In some people, these problems persist for over a year, especially those who had severe illness or ongoing inflammation.
Blood Markers Reveal Hidden Damage
Blood tests revealed important clues. Certain inflammatory cytokines such as IL-6, IL-1ß, TNFa, IL-8, and IL-13 remain elevated long after infection in people with brain fog. At the same time, proteins linked to brain cells and blood–brain barrier damage appear in the bloodstream, confirming that the brain’s protective system is affected.
While most patients show signs of recovery within six months, a smaller group continues to hav e ongoing inflammation and blood–brain barrier disruption, which strongly correlates with persistent cognitive symptoms.
Why These Findings Matter
This research highlights that post-COVID brain problems are real, measurable, and biologically driven. The findings suggest that early cognitive screening, long-term follow-up, and targeted brain rehabilitation are urgently needed. Ignoring these symptoms risks pushing patients into long-lasting cognitive decline that affects work, independence, and quality of life.
Conclusion
The study clearly shows that COVID-19 can cause long-term cognitive impairment through sustained inflammation and damage to the blood–brain barrier, even after the initial infection resolves. These findings emphasize the urgent need for long-term monitoring, early intervention, and specialized cognitive rehabilitation to prevent permanent mental health consequences in COVID-19 survivors.
The study findings were published in the peer reviewed International Journal of Molecular Sciences
COVID-19 Brain Fog Mystery Finally Explained
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 06, 2026
Medical News: Lingering Mental Effects After COVID-19 Raise New Alarms
Many people who have recovered from COVID-19 continue to complain about memory lapses, poor concentration, confusion, and what is commonly called “brain fog.” A major new scientific review now explains why these problems happen and why they can last for months or even years after infection. This Medical News report is based on an extensive analysis of existing research that examined how COVID-19 affects the blood-brain barrier and immune system over time.
The study was conducted by researchers from the Department of Clinical and Health Psychology, Universitat Autònoma de Barcelona, Spain, the Institut de Recerca Sant Joan de Déu, Spain, Universidad San Sebastián, Chile, CIBERSAM Biomedical Network Research Center of Mental Health, Spain, and the University of Vic–Central University of Catalonia, Spain.
How COVID-19 Triggers Brain Problems
The researchers found that COVID-19 does not need to directly infect the brain to cause cognitive issues. Instead, the virus triggers a powerful immune reaction in the body. This leads to high levels of inflammatory substances called cytokines circulating in the blood. These cytokines can weaken the blood–brain barrier, a protective layer that normally shields the brain from harmful substances.
Once this barrier is compromised, inflammatory signals can enter the brain, activating brain support cells and disrupting normal communication between nerve cells. This helps explain why many patients experience attention problems, memory loss, and slower thinking even after their lungs have healed.
Brain Fog Changes Over Time
The review showed that cognitive symptoms evolve in stages. During the first few weeks of infection, problems mainly affect attention, working memory, and decision-making. These early issues are usually linked to inflammation, low oxygen levels, and overall illness stress rather than permanent brain damage.
Between one and three months after infection, many patients still struggle with concentration and mental fatigue. By six months and beyond, a significant number develop broader cognitive difficulties involving multiple brain functions. In some people, these problems persist for over a year, especially those who had severe illness or ongoing inflammation.
Blood Markers Reveal Hidden Damage
Blood tests revealed important clues. Certain inflammatory cytokines such as IL-6, IL-1ß, TNFa, IL-8, and IL-13 remain elevated long after infection in people with brain fog. At the same time, proteins linked to brain cells and blood–brain barrier damage appear in the bloodstream, confirming that the brain’s protective system is affected.
While most patients show signs of recovery within six months, a smaller group continues to hav e ongoing inflammation and blood–brain barrier disruption, which strongly correlates with persistent cognitive symptoms.
Why These Findings Matter
This research highlights that post-COVID brain problems are real, measurable, and biologically driven. The findings suggest that early cognitive screening, long-term follow-up, and targeted brain rehabilitation are urgently needed. Ignoring these symptoms risks pushing patients into long-lasting cognitive decline that affects work, independence, and quality of life.
Conclusion
The study clearly shows that COVID-19 can cause long-term cognitive impairment through sustained inflammation and damage to the blood–brain barrier, even after the initial infection resolves. These findings emphasize the urgent need for long-term monitoring, early intervention, and specialized cognitive rehabilitation to prevent permanent mental health consequences in COVID-19 survivors.
The study findings were published in the peer reviewed International Journal of Molecular Sciences
Heliobas Disciple
TB Fanatic
(fair use applies)
Bromhexine and High Dose Colchicine Can Prevent and Treat Flu as Well as COVID-19 Infections
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
Medical News: A Fresh Look at Old Medicines for New Viral Threats
As the world continues to deal with recurring waves of COVID-19 and seasonal influenza, researchers are still searching for practical and affordable ways to prevent infections and reduce deaths. While certain antiviral drugs have helped to some extent, complications such as severe inflammation and organ failure remain a major concern. A recent scientific review has taken a different approach by closely examining two long-known and inexpensive medicines that together offer strong protection against both COVID-19 and influenza.
This Medical News report explores how bromhexine and colchicine, drugs that have been in use for decades, could play a key role in stopping viral infections early and preventing dangerous immune reactions later.
The research was led by scientists from the Research Institute of Innovative Medical Science, Department of Medical Chemistry and Biochemistry, Medical Faculty, Medical University Sofia in Bulgaria. The work was supported by national scientific funding bodies and reviewed according to established ethical standards.
Why COVID-19 and Influenza Are Still Dangerous
Despite advances in medicine, COVID-19 and influenza continue to claim lives worldwide. Influenza virus strains like H1N1 and H3N2 causes hundreds of thousands of deaths every year, while COVID-19 has resulted in millions of fatalities globally. Many severe cases do not occur simply because of the virus itself, but because the body’s immune system overreacts. This excessive reaction, often called a cytokine storm, can damage lungs, blood vessels, and vital organs.
The researchers focused on two key biological processes that are shared by both viruses. One process allows the virus to enter human cells. The other process triggers the intense inflammation that leads to severe illness and death.
Blocking the Virus Before It Enters Cells
Both influenza viruses and SARS-CoV-2 rely on a human enzyme called TMPRSS2 to enter cells in the respiratory tract. If this enzyme is blocked, the virus struggles to infect the body.
Bromhexine hydrochloride, widely used as a cough medicine for more than sixty years, was identified as an effective blocker of TMPRSS2. According to the review, bromhexine works best when taken before infection or immediately after exposure. When used in this preventive way, bromhexine can significantly reduce the chances of becoming infected. Even if infection occurs, symptoms tend to be much milder.
Importantly, bromhexine accumulates in lung tissues at levels high enough to block viral entry, while remaining safe and well tolerated. Researchers observed that people who took bromhexine regularly during high-risk periods were far less likely to become ill.
Stopping the Dangerous Immune Overreaction
Once the vi rus is inside the body, the main threat becomes uncontrolled inflammation. This is driven by a powerful immune structure known as the NLRP3 inflammasome. When overstimulated, it releases large amounts of inflammatory substances that can cause lung failure, blood clots, and damage to multiple organs.
Colchicine, a drug traditionally used to treat gout and inflammatory conditions, is known to suppress this inflammasome. However, the review highlights that many previous studies used colchicine doses that were too low to be effective. When higher, carefully monitored doses were used, the results were striking.
Patients treated with higher doses of colchicine showed significantly lower death rates, fewer hospitalizations, and faster recovery. In some studies, mortality dropped by up to seven times compared to standard care. Even among high-risk patients, including the elderly and those with obesity, outcomes improved dramatically.
Timing Is the Key to Success
One of the most important findings of the review is that timing matters more than almost anything else. Bromhexine is most effective when used early, before the virus enters cells. Colchicine is most effective when used during the critical phase of illness, just before or as severe inflammation begins.
Using antivirals alone or blocking only individual inflammatory molecules often fails because the underlying immune overreaction continues unchecked. The combined strategy of early prevention and later inflammation control appears to address both sides of the problem.
Safety and Cost Advantages
Both bromhexine and colchicine are inexpensive and widely available. Bromhexine has an excellent safety record, while colchicine’s main side effect at higher doses is temporary diarrhea. Serious liver damage or long-term harm was not observed when dosing guidelines were followed.
Compared to many newer antiviral drugs, these medicines are accessible even in low-resource settings, making them especially valuable during large outbreaks.
What This Means for the Future
The review suggests a shift in how doctors and health systems might approach respiratory viral outbreaks. Instead of relying only on vaccines and late-stage treatments, a proactive strategy using bromhexine for prevention and colchicine for complication control could save lives and reduce healthcare strain.
Conclusion
The findings strongly indicate that a combined approach using bromhexine to block viral entry and higher doses of colchicine to control harmful inflammation may offer a safe, affordable, and highly effective way to prevent severe COVID-19 and influenza outcomes. By targeting the root mechanisms of infection and immune overreaction, this strategy addresses major gaps left by current treatments and deserves serious attention from global health authorities and clinicians alike.
The study findings were published in the peer reviewed journal: Trends in Immunotherapy
Bromhexine and High Dose Colchicine Can Prevent and Treat Flu as Well as COVID-19 Infections
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
Medical News: A Fresh Look at Old Medicines for New Viral Threats
As the world continues to deal with recurring waves of COVID-19 and seasonal influenza, researchers are still searching for practical and affordable ways to prevent infections and reduce deaths. While certain antiviral drugs have helped to some extent, complications such as severe inflammation and organ failure remain a major concern. A recent scientific review has taken a different approach by closely examining two long-known and inexpensive medicines that together offer strong protection against both COVID-19 and influenza.
This Medical News report explores how bromhexine and colchicine, drugs that have been in use for decades, could play a key role in stopping viral infections early and preventing dangerous immune reactions later.
The research was led by scientists from the Research Institute of Innovative Medical Science, Department of Medical Chemistry and Biochemistry, Medical Faculty, Medical University Sofia in Bulgaria. The work was supported by national scientific funding bodies and reviewed according to established ethical standards.
Why COVID-19 and Influenza Are Still Dangerous
Despite advances in medicine, COVID-19 and influenza continue to claim lives worldwide. Influenza virus strains like H1N1 and H3N2 causes hundreds of thousands of deaths every year, while COVID-19 has resulted in millions of fatalities globally. Many severe cases do not occur simply because of the virus itself, but because the body’s immune system overreacts. This excessive reaction, often called a cytokine storm, can damage lungs, blood vessels, and vital organs.
The researchers focused on two key biological processes that are shared by both viruses. One process allows the virus to enter human cells. The other process triggers the intense inflammation that leads to severe illness and death.
Blocking the Virus Before It Enters Cells
Both influenza viruses and SARS-CoV-2 rely on a human enzyme called TMPRSS2 to enter cells in the respiratory tract. If this enzyme is blocked, the virus struggles to infect the body.
Bromhexine hydrochloride, widely used as a cough medicine for more than sixty years, was identified as an effective blocker of TMPRSS2. According to the review, bromhexine works best when taken before infection or immediately after exposure. When used in this preventive way, bromhexine can significantly reduce the chances of becoming infected. Even if infection occurs, symptoms tend to be much milder.
Importantly, bromhexine accumulates in lung tissues at levels high enough to block viral entry, while remaining safe and well tolerated. Researchers observed that people who took bromhexine regularly during high-risk periods were far less likely to become ill.
Stopping the Dangerous Immune Overreaction
Once the vi rus is inside the body, the main threat becomes uncontrolled inflammation. This is driven by a powerful immune structure known as the NLRP3 inflammasome. When overstimulated, it releases large amounts of inflammatory substances that can cause lung failure, blood clots, and damage to multiple organs.
Colchicine, a drug traditionally used to treat gout and inflammatory conditions, is known to suppress this inflammasome. However, the review highlights that many previous studies used colchicine doses that were too low to be effective. When higher, carefully monitored doses were used, the results were striking.
Patients treated with higher doses of colchicine showed significantly lower death rates, fewer hospitalizations, and faster recovery. In some studies, mortality dropped by up to seven times compared to standard care. Even among high-risk patients, including the elderly and those with obesity, outcomes improved dramatically.
Timing Is the Key to Success
One of the most important findings of the review is that timing matters more than almost anything else. Bromhexine is most effective when used early, before the virus enters cells. Colchicine is most effective when used during the critical phase of illness, just before or as severe inflammation begins.
Using antivirals alone or blocking only individual inflammatory molecules often fails because the underlying immune overreaction continues unchecked. The combined strategy of early prevention and later inflammation control appears to address both sides of the problem.
Safety and Cost Advantages
Both bromhexine and colchicine are inexpensive and widely available. Bromhexine has an excellent safety record, while colchicine’s main side effect at higher doses is temporary diarrhea. Serious liver damage or long-term harm was not observed when dosing guidelines were followed.
Compared to many newer antiviral drugs, these medicines are accessible even in low-resource settings, making them especially valuable during large outbreaks.
What This Means for the Future
The review suggests a shift in how doctors and health systems might approach respiratory viral outbreaks. Instead of relying only on vaccines and late-stage treatments, a proactive strategy using bromhexine for prevention and colchicine for complication control could save lives and reduce healthcare strain.
Conclusion
The findings strongly indicate that a combined approach using bromhexine to block viral entry and higher doses of colchicine to control harmful inflammation may offer a safe, affordable, and highly effective way to prevent severe COVID-19 and influenza outcomes. By targeting the root mechanisms of infection and immune overreaction, this strategy addresses major gaps left by current treatments and deserves serious attention from global health authorities and clinicians alike.
The study findings were published in the peer reviewed journal: Trends in Immunotherapy
Heliobas Disciple
TB Fanatic
(fair use applies)
Deadly COVID-19 and Flu Coinfection Sparks Heart and Brain Attacks
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
A newly published medical case from Taiwan has revealed how a rare but dangerous combination of COVID-19 and influenza A can trigger life threatening complications affecting both the heart and the brain. This alarming case highlights the hidden dangers of viral coinfections that many people may underestimate, even as the global focus on COVID-19 fades.
A Rare and Dangerous Combination
Researchers from the Division of Infectious Diseases and Tropical Medicine Department of Medicine Tri Service General Hospital National Defense Medical University Taipei Taiwan documented the case of a 75-year-old woman who was infected with both SARS-CoV-2 and influenza A at the same time. While each virus alone is known to cause serious illness, their coexistence created a perfect storm inside the body.
This Medical News report explains that the woman initially arrived at the hospital with common symptoms such as fever cough and weakness. However, within days her condition worsened dramatically. She developed breathing failure followed by sudden weakness on one side of her body and reduced consciousness signs that something far more severe was happening.
How The Viruses Triggered Clots
Doctors discovered that the patient suffered two major events almost simultaneously a heart attack and a stroke. This rare condition is known as cardio cerebral infarction and is considered a medical emergency with high risks of death or permanent disability.
Tests showed that both viruses had caused intense inflammation in the blood vessels. This inflammation made the blood unusually sticky increasing the risk of dangerous clots forming. In this case clots blocked blood flow to the heart causing a heart attack and also blocked blood flow to parts of the brain leading to a stroke.
The study explains that COVID-19 is already linked to abnormal clotting while influenza can inflame blood vessels. Together they appear to amplify each other making severe complications more likely especially in older adults or those with conditions like diabetes or high blood pressure.
Life Saving Interventions
Doctors acted quickly using antiviral drugs steroids and breathing support. When heart damage was confirmed, the patient underwent an emergency procedure to open a blocked heart artery and received dual antiplatelet medicines to prevent further clots. Brain scans confirmed fresh areas of stroke but careful treatment helped avoid bleeding complications.
After a month of intensive care and rehabilitation the patient survived and recovered with only mild weakness remaining.
Why This Case Matters
This is the first documented case of simultaneous heart attack and stroke linked specifically to coinfection with COVID 19 and influenza A. The researchers warn that such coinfections may lead to more severe ou tcomes than either virus alone and can complicate treatment decisions for doctors.
Key Takeaways and Conclusions
The findings strongly suggest that viral coinfections can dramatically increase the risk of blood clots affecting vital organs. Early recognition aggressive monitoring and preventive clot management may save lives. Even though COVID 19 is no longer classified as a global emergency doctors and the public must remain alert to the dangers posed by overlapping respiratory infections particularly during flu seasons.
The study findings were published in the peer reviewed journal: Infection and Drug Resistance
Deadly COVID-19 and Flu Coinfection Sparks Heart and Brain Attacks
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
A newly published medical case from Taiwan has revealed how a rare but dangerous combination of COVID-19 and influenza A can trigger life threatening complications affecting both the heart and the brain. This alarming case highlights the hidden dangers of viral coinfections that many people may underestimate, even as the global focus on COVID-19 fades.
A Rare and Dangerous Combination
Researchers from the Division of Infectious Diseases and Tropical Medicine Department of Medicine Tri Service General Hospital National Defense Medical University Taipei Taiwan documented the case of a 75-year-old woman who was infected with both SARS-CoV-2 and influenza A at the same time. While each virus alone is known to cause serious illness, their coexistence created a perfect storm inside the body.
This Medical News report explains that the woman initially arrived at the hospital with common symptoms such as fever cough and weakness. However, within days her condition worsened dramatically. She developed breathing failure followed by sudden weakness on one side of her body and reduced consciousness signs that something far more severe was happening.
How The Viruses Triggered Clots
Doctors discovered that the patient suffered two major events almost simultaneously a heart attack and a stroke. This rare condition is known as cardio cerebral infarction and is considered a medical emergency with high risks of death or permanent disability.
Tests showed that both viruses had caused intense inflammation in the blood vessels. This inflammation made the blood unusually sticky increasing the risk of dangerous clots forming. In this case clots blocked blood flow to the heart causing a heart attack and also blocked blood flow to parts of the brain leading to a stroke.
The study explains that COVID-19 is already linked to abnormal clotting while influenza can inflame blood vessels. Together they appear to amplify each other making severe complications more likely especially in older adults or those with conditions like diabetes or high blood pressure.
Life Saving Interventions
Doctors acted quickly using antiviral drugs steroids and breathing support. When heart damage was confirmed, the patient underwent an emergency procedure to open a blocked heart artery and received dual antiplatelet medicines to prevent further clots. Brain scans confirmed fresh areas of stroke but careful treatment helped avoid bleeding complications.
After a month of intensive care and rehabilitation the patient survived and recovered with only mild weakness remaining.
Why This Case Matters
This is the first documented case of simultaneous heart attack and stroke linked specifically to coinfection with COVID 19 and influenza A. The researchers warn that such coinfections may lead to more severe ou tcomes than either virus alone and can complicate treatment decisions for doctors.
Key Takeaways and Conclusions
The findings strongly suggest that viral coinfections can dramatically increase the risk of blood clots affecting vital organs. Early recognition aggressive monitoring and preventive clot management may save lives. Even though COVID 19 is no longer classified as a global emergency doctors and the public must remain alert to the dangers posed by overlapping respiratory infections particularly during flu seasons.
The study findings were published in the peer reviewed journal: Infection and Drug Resistance
Heliobas Disciple
TB Fanatic
(fair use applies)
COVID-19 is Causing Impaired Nutrient Absorption in Many Individuals
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
In the wake of the global COVID-19 pandemic, emerging research has uncovered a hidden toll on the human body beyond the well-known respiratory symptoms. Scientists are increasingly recognizing that SARS-CoV-2, the virus responsible for COVID-19, can significantly disrupt the gastrointestinal system, leading to impaired nutrient absorption in many patients. This issue affects not only those with severe cases but also individuals experiencing mild infections or long-term post-COVID symptoms. Peer-reviewed studies highlight how the virus targets the gut, causing widespread damage that hampers the body's ability to extract essential vitamins, minerals, and other nutrients from food.
This Medical News report delves into the mechanisms behind this phenomenon, drawing from recent scientific investigations. As the world continues to grapple with the virus's long-term effects, understanding these gastrointestinal impacts is crucial for developing targeted interventions and improving patient outcomes.
Intestinal Damage Caused by SARS-CoV-2
SARS-CoV-2 enters the body primarily through the respiratory tract but can also invade the gastrointestinal system via the angiotensin-converting enzyme 2 (ACE2) receptor, which is abundantly expressed on intestinal epithelial cells. This binding leads to direct cytopathic effects, causing cell damage and apoptosis of enterocytes—the cells responsible for nutrient absorption in the small intestine.
The virus triggers an inflammatory response, releasing pro-inflammatory cytokines like IL-6 and TNF-alpha, which further exacerbate tissue injury. Studies show that this results in thickened bowel walls, increased permeability (often called "leaky gut"), and even ischemia in severe cases.
One key mechanism involves the downregulation of ACE2, which normally regulates intestinal homeostasis. When SARS-CoV-2 binds to ACE2, it impairs the function of associated transporters like B0AT1, essential for absorbing amino acids such as tryptophan.
This disruption not only affects nutrient uptake but also weakens the gut's barrier integrity, allowing harmful substances to enter the bloodstream and trigger systemic inflammation. Autopsy and biopsy studies from COVID-19 patients reveal histopathological changes, including villous atrophy and endothelial damage, mirroring conditions like celiac disease or inflammatory bowel disease.
Gut Dysbiosis and Its Role in Disease Progression
COVID-19 infection profoundly alters the gut microbiome, leading to dysbiosis—a state of microbial imbalance characterized by a decline in beneficial bacteria and an overgrowth of opportunistic pathogens.
Beneficial species such as Faecalibacterium prausnitzii, Bifidobacterium, and Eubacterium—known for producing short-chain fatty acids (SCFAs) like butyr ate—are depleted in infected individuals.
These SCFAs are vital for maintaining the intestinal barrier, regulating immune responses, and promoting nutrient absorption. Conversely, pathogens like Enterococcus, Streptococcus, and Escherichia coli proliferate, contributing to inflammation and further barrier dysfunction.
This dysbiosis persists even after viral clearance, correlating with disease severity and the development of post-acute sequelae of COVID-19 (PASC), or long COVID. Factors exacerbating dysbiosis include antibiotic use during treatment, systemic hypoxia from lung damage, and reduced caloric intake due to illness-induced anorexia.
The altered microbiome reduces SCFA production, which impairs epithelial cell regeneration and increases gut permeability, allowing bacterial endotoxins to translocate into the blood, fueling a cytokine storm.
Mechanisms Leading to Impaired Nutrient Absorption
The interplay between intestinal damage and dysbiosis directly impairs nutrient absorption through multiple pathways. Damaged enterocytes lose their brush border enzymes and transporters, reducing the uptake of carbohydrates, proteins, fats, and micronutrients like vitamins B12, D, and iron.
For instance, tryptophan malabsorption disrupts serotonin production and antimicrobial peptide expression, further perpetuating dysbiosis in a vicious cycle. Leaky gut syndrome allows undigested food particles and toxins to enter circulation, triggering immune activation that diverts energy from absorption processes.
Studies indicate that COVID-19 patients often exhibit deficiencies in zinc, selenium, and vitamin D, which are exacerbated by poor absorption rather than just dietary insufficiency.
Additionally, the virus's impact on the enteric nervous system can alter gut motility, leading to diarrhea or constipation, which further hinders nutrient extraction. In severe cases, systemic effects like coagulopathy and thromboembolism can cause ischemic damage to the gut, compounding absorption issues.
Research also links these changes to metabolic disruptions, such as impaired mTOR pathway signaling, which regulates cellular nutrient sensing and autophagy.
Long-Term Implications for Health
The consequences of impaired nutrient absorption extend far beyond the acute phase of COVID-19. Many survivors report persistent fatigue, muscle weakness, and cognitive issues—symptoms potentially tied to chronic malnutrition from ongoing gut dysfunction.
Dysbiosis has been associated with increased risk of secondary infections, autoimmune conditions, and even skin disorders due to systemic inflammation.
Interventions like probiotics, prebiotics, and fecal microbiota transplants are being explored to restore gut balance and improve absorption.
However, more research is needed to tailor these therapies, especially in regions where dietary habits and microbiome profiles may differ.
In conclusion, COVID-19's assault on the gut underscores the need for holistic approaches to recovery, including nutritional support and microbiome monitoring. By addressing these hidden effects, healthcare providers can mitigate long-term health burdens for millions affected worldwide.
References:
https://www.sciencedirect.com/science/article/pii/S2405457724000469
https://www.clinicalnutritionjournal.com/article/S0261-5614(22)00277-1/fulltext
https://www.cghjournal.org/article/S1542-3565(22)01004-7/pdf
https://www.sciencedirect.com/science/article/pii/S1043466622000357
https://www.mdpi.com/2227-9059/11/4/1014
Frontiers | Intestinal Damage in COVID-19: SARS-CoV-2 Infection and Intestinal Thrombosis
https://www.wjgnet.com/2307-8960/full/v11/i22/5252.htm
https://www.wjgnet.com/1007-9327/full/v29/i15/2283.htm
Frontiers | Microbiome dysbiosis in SARS-CoV-2 infection: implication for pathophysiology and management strategies of COVID-19
https://www.mdpi.com/2673-8112/5/4/48
Gut microbiota in COVID-19: key microbial changes, potential mechanisms and clinical applications - Nature Reviews Gastroenterology & Hepatology
Impact of SARS-CoV2 infection on gut microbiota dysbiosis
https://www.sciencedirect.com/science/article/pii/S0985056222000255
https://www.tandfonline.com/doi/full/10.1080/19490976.2023.2201157
https://www.wjgnet.com/2220-3249/full/v12/i2/68.htm
Frontiers | COVID-19 influenced gut dysbiosis, post-acute sequelae, immune regulation, and therapeutic regimens
COVID-19 is Causing Impaired Nutrient Absorption in Many Individuals
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 05, 2026
In the wake of the global COVID-19 pandemic, emerging research has uncovered a hidden toll on the human body beyond the well-known respiratory symptoms. Scientists are increasingly recognizing that SARS-CoV-2, the virus responsible for COVID-19, can significantly disrupt the gastrointestinal system, leading to impaired nutrient absorption in many patients. This issue affects not only those with severe cases but also individuals experiencing mild infections or long-term post-COVID symptoms. Peer-reviewed studies highlight how the virus targets the gut, causing widespread damage that hampers the body's ability to extract essential vitamins, minerals, and other nutrients from food.
This Medical News report delves into the mechanisms behind this phenomenon, drawing from recent scientific investigations. As the world continues to grapple with the virus's long-term effects, understanding these gastrointestinal impacts is crucial for developing targeted interventions and improving patient outcomes.
Intestinal Damage Caused by SARS-CoV-2
SARS-CoV-2 enters the body primarily through the respiratory tract but can also invade the gastrointestinal system via the angiotensin-converting enzyme 2 (ACE2) receptor, which is abundantly expressed on intestinal epithelial cells. This binding leads to direct cytopathic effects, causing cell damage and apoptosis of enterocytes—the cells responsible for nutrient absorption in the small intestine.
The virus triggers an inflammatory response, releasing pro-inflammatory cytokines like IL-6 and TNF-alpha, which further exacerbate tissue injury. Studies show that this results in thickened bowel walls, increased permeability (often called "leaky gut"), and even ischemia in severe cases.
One key mechanism involves the downregulation of ACE2, which normally regulates intestinal homeostasis. When SARS-CoV-2 binds to ACE2, it impairs the function of associated transporters like B0AT1, essential for absorbing amino acids such as tryptophan.
This disruption not only affects nutrient uptake but also weakens the gut's barrier integrity, allowing harmful substances to enter the bloodstream and trigger systemic inflammation. Autopsy and biopsy studies from COVID-19 patients reveal histopathological changes, including villous atrophy and endothelial damage, mirroring conditions like celiac disease or inflammatory bowel disease.
Gut Dysbiosis and Its Role in Disease Progression
COVID-19 infection profoundly alters the gut microbiome, leading to dysbiosis—a state of microbial imbalance characterized by a decline in beneficial bacteria and an overgrowth of opportunistic pathogens.
Beneficial species such as Faecalibacterium prausnitzii, Bifidobacterium, and Eubacterium—known for producing short-chain fatty acids (SCFAs) like butyr ate—are depleted in infected individuals.
These SCFAs are vital for maintaining the intestinal barrier, regulating immune responses, and promoting nutrient absorption. Conversely, pathogens like Enterococcus, Streptococcus, and Escherichia coli proliferate, contributing to inflammation and further barrier dysfunction.
This dysbiosis persists even after viral clearance, correlating with disease severity and the development of post-acute sequelae of COVID-19 (PASC), or long COVID. Factors exacerbating dysbiosis include antibiotic use during treatment, systemic hypoxia from lung damage, and reduced caloric intake due to illness-induced anorexia.
The altered microbiome reduces SCFA production, which impairs epithelial cell regeneration and increases gut permeability, allowing bacterial endotoxins to translocate into the blood, fueling a cytokine storm.
Mechanisms Leading to Impaired Nutrient Absorption
The interplay between intestinal damage and dysbiosis directly impairs nutrient absorption through multiple pathways. Damaged enterocytes lose their brush border enzymes and transporters, reducing the uptake of carbohydrates, proteins, fats, and micronutrients like vitamins B12, D, and iron.
For instance, tryptophan malabsorption disrupts serotonin production and antimicrobial peptide expression, further perpetuating dysbiosis in a vicious cycle. Leaky gut syndrome allows undigested food particles and toxins to enter circulation, triggering immune activation that diverts energy from absorption processes.
Studies indicate that COVID-19 patients often exhibit deficiencies in zinc, selenium, and vitamin D, which are exacerbated by poor absorption rather than just dietary insufficiency.
Additionally, the virus's impact on the enteric nervous system can alter gut motility, leading to diarrhea or constipation, which further hinders nutrient extraction. In severe cases, systemic effects like coagulopathy and thromboembolism can cause ischemic damage to the gut, compounding absorption issues.
Research also links these changes to metabolic disruptions, such as impaired mTOR pathway signaling, which regulates cellular nutrient sensing and autophagy.
Long-Term Implications for Health
The consequences of impaired nutrient absorption extend far beyond the acute phase of COVID-19. Many survivors report persistent fatigue, muscle weakness, and cognitive issues—symptoms potentially tied to chronic malnutrition from ongoing gut dysfunction.
Dysbiosis has been associated with increased risk of secondary infections, autoimmune conditions, and even skin disorders due to systemic inflammation.
Interventions like probiotics, prebiotics, and fecal microbiota transplants are being explored to restore gut balance and improve absorption.
However, more research is needed to tailor these therapies, especially in regions where dietary habits and microbiome profiles may differ.
In conclusion, COVID-19's assault on the gut underscores the need for holistic approaches to recovery, including nutritional support and microbiome monitoring. By addressing these hidden effects, healthcare providers can mitigate long-term health burdens for millions affected worldwide.
References:
https://www.sciencedirect.com/science/article/pii/S2405457724000469
https://www.clinicalnutritionjournal.com/article/S0261-5614(22)00277-1/fulltext
https://www.cghjournal.org/article/S1542-3565(22)01004-7/pdf
https://www.sciencedirect.com/science/article/pii/S1043466622000357
https://www.mdpi.com/2227-9059/11/4/1014
Frontiers | Intestinal Damage in COVID-19: SARS-CoV-2 Infection and Intestinal Thrombosis
https://www.wjgnet.com/2307-8960/full/v11/i22/5252.htm
https://www.wjgnet.com/1007-9327/full/v29/i15/2283.htm
Frontiers | Microbiome dysbiosis in SARS-CoV-2 infection: implication for pathophysiology and management strategies of COVID-19
https://www.mdpi.com/2673-8112/5/4/48
Gut microbiota in COVID-19: key microbial changes, potential mechanisms and clinical applications - Nature Reviews Gastroenterology & Hepatology
Impact of SARS-CoV2 infection on gut microbiota dysbiosis
https://www.sciencedirect.com/science/article/pii/S0985056222000255
https://www.tandfonline.com/doi/full/10.1080/19490976.2023.2201157
https://www.wjgnet.com/2220-3249/full/v12/i2/68.htm
Frontiers | COVID-19 influenced gut dysbiosis, post-acute sequelae, immune regulation, and therapeutic regimens
Heliobas Disciple
TB Fanatic
(fair use applies)
COVID-19 still claims more than 100,000 US lives each year
by Justin Jackson, Medical Xpress
edited by Sadie Harley, reviewed by Robert Egan
January 7, 2026
Centers for Disease Control and Prevention researchers report national estimates of 43.6 million COVID-19-associated illnesses and 101,300 deaths in the US during October 2022 to September 2023, plus 33.0 million illnesses and 100,800 deaths during October 2023 to September 2024. People 65 years and older accounted for the majority of hospitalizations and deaths.
COVID-19 has continued to affect the US health care system through outpatient visits, hospitalizations, and deaths long after the public health emergency declaration ended in May 2023. SARS-CoV-2 circulation has added pressure during winter respiratory illness seasons while other respiratory viruses continue to circulate.
Current estimates feed decisions on resource allocation and public health policy, but they cannot react to what they cannot see. Case reporting to the US Centers for Disease Control and Prevention ended with the end of the COVID-19 public health emergency, removing a national stream of case-based data used earlier in the pandemic.
Mortality tracking often relies on death certificates listing COVID-19 as an underlying or contributing cause of death. Relaxed reporting requirements, new variants, and reduced testing complicate estimates of disease burden. Even symptomatic people often do not seek care or testing, creating gaps in attributable illness and death.
In the study, "Estimated Burden of COVID-19 Illnesses, Medical Visits, Hospitalizations, and Deaths in the US From October 2022 to September 2024," published in JAMA Internal Medicine, researchers applied hierarchical Bayesian modeling and probabilistic mathematical multiplier models to estimate COVID-19-associated illnesses, outpatient visits, hospitalizations, and deaths in the US from October 2022 to September 2024.
COVID-19 Hospitalization Surveillance Network (COVID-NET) data came from 89 counties and jurisdictional equivalents in 12 states, covering approximately 10% of the US population. Data included 94,363 participants for October 2022 to September 2023 and 72,176 participants for October 2023 to September 2024.
Concentration of severe outcomes
During the 2022–2023 period, there were an estimated 43.6 million COVID-19-associated illnesses, 10.0 million outpatient visits, 1.1 million hospitalizations, and 101,300 deaths.
During the 2023–2024 period, there were an estimated 33.0 million COVID-19-associated illnesses, 7.7 million outpatient visits, 879,100 hospitalizations, and 100,800 deaths.
Adults aged 65 years and older made up 17.7% of the total US population during 2023–2024 and accounted for 47.9% of COVID-19-associated illnesses. 65 and older accounted for 64.3% of COVID-19-associated outpatient visits, 67.6% of associated hospitalizations, and 81.2% of deaths.
Prevention and treatment gaps
Vaccination and early antiviral treatment may prevent severe COVID-19 consequences. Estimates in 2024 indicate 18% of US adults aged 18 years and older and 30% of nursing home residents received a recent COVID-19 vaccine. Outpatient antiviral treatment in 2024 reached fewer than one-half of adults aged 65 years and older.
Assumptions can begin to shape personal choices as well as national policy when a surveillance network stops reporting and there is a real danger that people will assume the risk is gone. COVID-19 hasn't gone away, and vaccines are still actively preventing severe illness and death.
More information
Emilia H. A. Koumans et al, Estimated Burden of COVID-19 Illnesses, Medical Visits, Hospitalizations, and Deaths in the US From October 2022 to September 2024, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2025.7179
David C. Grabowski, The Continuing Burden of COVID-19 on Older Adults, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2025.7187
Journal information: JAMA Internal Medicine
Key medical concepts
COVID-19 (Coronavirus Disease 2019) Vaccination SARS-CoV-2
COVID-19 still claims more than 100,000 US lives each year
by Justin Jackson, Medical Xpress
edited by Sadie Harley, reviewed by Robert Egan
January 7, 2026
Centers for Disease Control and Prevention researchers report national estimates of 43.6 million COVID-19-associated illnesses and 101,300 deaths in the US during October 2022 to September 2023, plus 33.0 million illnesses and 100,800 deaths during October 2023 to September 2024. People 65 years and older accounted for the majority of hospitalizations and deaths.
COVID-19 has continued to affect the US health care system through outpatient visits, hospitalizations, and deaths long after the public health emergency declaration ended in May 2023. SARS-CoV-2 circulation has added pressure during winter respiratory illness seasons while other respiratory viruses continue to circulate.
Current estimates feed decisions on resource allocation and public health policy, but they cannot react to what they cannot see. Case reporting to the US Centers for Disease Control and Prevention ended with the end of the COVID-19 public health emergency, removing a national stream of case-based data used earlier in the pandemic.
Mortality tracking often relies on death certificates listing COVID-19 as an underlying or contributing cause of death. Relaxed reporting requirements, new variants, and reduced testing complicate estimates of disease burden. Even symptomatic people often do not seek care or testing, creating gaps in attributable illness and death.
In the study, "Estimated Burden of COVID-19 Illnesses, Medical Visits, Hospitalizations, and Deaths in the US From October 2022 to September 2024," published in JAMA Internal Medicine, researchers applied hierarchical Bayesian modeling and probabilistic mathematical multiplier models to estimate COVID-19-associated illnesses, outpatient visits, hospitalizations, and deaths in the US from October 2022 to September 2024.
COVID-19 Hospitalization Surveillance Network (COVID-NET) data came from 89 counties and jurisdictional equivalents in 12 states, covering approximately 10% of the US population. Data included 94,363 participants for October 2022 to September 2023 and 72,176 participants for October 2023 to September 2024.
Concentration of severe outcomes
During the 2022–2023 period, there were an estimated 43.6 million COVID-19-associated illnesses, 10.0 million outpatient visits, 1.1 million hospitalizations, and 101,300 deaths.
During the 2023–2024 period, there were an estimated 33.0 million COVID-19-associated illnesses, 7.7 million outpatient visits, 879,100 hospitalizations, and 100,800 deaths.
Adults aged 65 years and older made up 17.7% of the total US population during 2023–2024 and accounted for 47.9% of COVID-19-associated illnesses. 65 and older accounted for 64.3% of COVID-19-associated outpatient visits, 67.6% of associated hospitalizations, and 81.2% of deaths.
Prevention and treatment gaps
Vaccination and early antiviral treatment may prevent severe COVID-19 consequences. Estimates in 2024 indicate 18% of US adults aged 18 years and older and 30% of nursing home residents received a recent COVID-19 vaccine. Outpatient antiviral treatment in 2024 reached fewer than one-half of adults aged 65 years and older.
Assumptions can begin to shape personal choices as well as national policy when a surveillance network stops reporting and there is a real danger that people will assume the risk is gone. COVID-19 hasn't gone away, and vaccines are still actively preventing severe illness and death.
More information
Emilia H. A. Koumans et al, Estimated Burden of COVID-19 Illnesses, Medical Visits, Hospitalizations, and Deaths in the US From October 2022 to September 2024, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2025.7179
David C. Grabowski, The Continuing Burden of COVID-19 on Older Adults, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2025.7187
Journal information: JAMA Internal Medicine
Key medical concepts
COVID-19 (Coronavirus Disease 2019) Vaccination SARS-CoV-2
Heliobas Disciple
TB Fanatic
Researchers Find Residual DNA in mRNA COVID Vaccines. Standard Testing Didn't Detect It.
A new study partially funded by Children’s Health Defense found residual DNA in Pfizer and Moderna COVID-19 mRNA vaccines. Current methods recommended by regulators and used by vaccine makers substantially underestimate DNA contamination, according to the researchers, who said better, more...
childrenshealthdefense.org
Researchers Find Residual DNA, Not Detected by Standard Tests, in mRNA COVID Vaccines
A new study partially funded by Children’s Health Defense found residual DNA in Pfizer and Moderna COVID-19 mRNA vaccines. Current methods recommended by regulators and used by vaccine makers substantially underestimate DNA contamination, according to the researchers, who said better, more accurate testing methods exist and should be mandated.
by Brenda Baletti, Ph.D.
January 12, 2026
A new laboratory analysis of commercially available mRNA COVID-19 vaccines found that residual DNA fragments — including sequences linked to the spike protein gene — remain in the final vaccine products.
According to the researchers, the DNA fragments exist in forms that standard regulatory testing methods don’t typically detect.
The researchers concluded that commonly used quality-control tests can underestimate total residual DNA by more than 100-fold, because the tests fail to detect DNA bound in RNA : DNA hybrid structures.
The study, published in a preprint authored by Kevin McKernan, Charles Rixey and Jessica Rose, Ph.D., examined unopened, “cold-chain compliant” Pfizer and Moderna vaccine vials using multiple analytical techniques.
Brian Hooker, Ph.D., chief scientific officer for Children’s Health Defense, which partially funded the research, told The Defender that having this type of genetic code in the vaccines’ lipid nanoparticles, which can easily cross cell membranes, is “dangerous indeed.”
When the vaccines were designed, the code for the spike protein was meant to express itself in the body in a targeted location for only about two weeks, Hooker said.
“However, this exogenous DNA can more easily disperse through the body and continue to both replicate and express episomally, making humans into genetically modified spike protein production factories,” Hooker said.
Hooker said the study may help explain some widespread clinical findings, “given that some vaccinated patients have been reported to continue to produce spike protein for periods as long as two years following their last COVID shot. This doesn’t even include the insertional effects that this additional exogenous DNA may have, leading to many different disorders, including cancer.”
Manufacturers ‘must have known’ residual DNA remained present
McKernan, chief scientific officer and founder of Medicinal Genomics, first raised concerns over DNA contamination in COVID-19 vaccines in 2023. That’s when his lab sequenced Moderna and Pfizer’s COVID-19 vaccines and found the presence of residual DNA that he accused Pfizer of deleting from the data the company gave regulators.
McKernan’s lab tested the vaccines and found that instead of containing only mRNA, the Pfizer vaccines also contained DNA plasmids — small, circular, double-stranded DNA molecules distinct from a cell’s chromosomal DNA.
McKernan explained that to manufacture mRNA vaccines, labs use a process called “in vitro transcription” to produce the necessary RNA molecules.
To produce the RNA molecules, the scientists design a DNA template that triggers the production of the RNA sequence they want. An enzyme that recognizes this signal then copies the DNA into RNA.
However, to function properly, the DNA in the template needs to be amplified. For the clinical trials, Pfizer amplified DNA using PCR (polymerase chain reaction), a method it called “Process 1,” which created a clean version of DNA to make the RNA.
However, Process 1 was expensive. So to mass-produce vaccines for the public, Pfizer used “Process 2,” which used a different method to amplify the DNA. Process 2 is cheaper and easier, but runs the risk of introducing sequences that weren’t present in the original DNA.
McKernan called this switch from Process 1 to Process 2 a “bait and switch.” In a recent Substack video, he said the change was “a premeditated move.”
“You can tell what their intentions are by what assays they built,” he said. “And you can see by what they did that their plan from the start was to always use Process 2.”
Manufacturers are required to digest and remove those sequences, which they did in this case using an enzyme called deoxyribonuclease or DNase.
However, in the preprint study, the researchers reported that in all cases they examined, the enzyme didn’t completely destroy the sequences.
“We proved a theory as to why and how the DNA got into the Moderna and Pfizer vials, in this new paper,” co-author Rose told The Defender. “There is DNA in every single vial tested to date. This has been reproduced in multiple labs across the world using multiple techniques. And the DNA came from hybridized RNA : DNA as a part of the Process 2 up-scaling process.”
Rose added:
“These hybrids were not degradable by the enzyme the manufacturers chose to use to clean out residual DNA as the final step in the process, and they must have known this because it is known in the space that the enzyme they selected does not degrade hybrids. It’s scandalous what they did.”
Regulators use wrong safety limit, wrong tool to look for DNA fragments
Regulatory guidance generally limits residual DNA to 10 nanograms per dose. However, the authors said DNase does not digest all DNA equally.
On Substack, McKernan explained the 10-nanogram limit is outdated because it was created based on the assumption that residual DNA is “naked DNA,” which degrades quickly. But the DNA in COVID-19 vaccines is encapsulated in the lipid nanoparticle, so it doesn’t degrade as fast.
The safety issue with COVID-19 vaccines isn’t related to the weight, but to the number of DNA fragments — more fragments present a greater risk for that DNA to be integrated into existing cells.
Some DNA sequences hybridize with their corresponding RNA transcripts, which carry genetic information from DNA used for building proteins. These RNA : DNA hybrids are significantly more resistant to “DNase I digestion” than typical double-stranded DNA, according to the authors.
Because the spike gene region is transcribed into mRNA in large quantities, it is particularly prone to forming such hybrids.
Even though manufacturers are aware of this issue, regulatory testing typically relies on a single lab technique that amplifies and measures a specific DNA sequence, called a “qPCR assay.” That method is used only to target the kanamycin (KAN) resistance gene — a plasmid region that is not transcribed and is highly sensitive to DNase digestion.
According to the study, this approach creates a systematic bias: the DNA that is easiest to destroy is also the DNA that is measured, while more resistant regions go largely uncounted.
On Substack, McKernan said this was by design. “The assays they designed were designed not to find things.”
CHD Senior Research Scientist Karl Jablonowski said, “Regulators leveraged ‘just one assay target for vaccine sponsor quality control. They didn’t verify quality, nor did a third party.”
Because of that approach, “Those who stood to profit from the vaccines designed the test and tested the quality,” Jablonowski said. “They chose a test that was least likely to yield a bad outcome. A perfectly usable and validated alternative was already in their toolbox, but the results may have halted the entire enterprise.”
DNA levels vary by more than 100-fold depending on the test used
The researchers compared qPCR tests targeting different plasmid regions, rather than just the KAN region. They found discrepancies exceeding 100-fold in measured DNA concentration in the different plasmid regions.
Tests that targeted the spike protein consistently detected far more residual DNA than tests that targeted the KAN gene or other locations.
Fluorometric measurements — a different type of test that detects substances by targeting them with fluorescent light — showed DNA levels ranging from 15 to 48 times higher than the U.S. Food and Drug Administration’s recommended limit across all tested vaccine lots.
The authors tested whether RNA : DNA hybrids were responsible for the discrepancy, and found evidence that they were.
They also had an independent company, Oxford Nanopore Technologies, confirm the presence of long DNA molecules. Longer molecules are more likely to be expressed by host cells than smaller ones, they noted.
The researchers concluded that much of the residual DNA detected in the vaccines exists in hybridized forms that resist the very enzyme specified for eliminating residual DNA in current manufacturing guidance, and that the type of test used will likely not detect residual DNA.
Authors question regulatory process, call for changes
The authors conclude that current regulatory reliance on a single, DNase-sensitive qPCR target is not adequate for identifying DNA impurities in mRNA therapeutics. Its use led regulators to “systematically underestimate the total burden of residual plasmid DNA.”
Instead, they recommend regulators mandate a multi-method approach that includes RNase-controlled fluorometry, testing multiple qPCR targets in different regions, and sequencing for fragment characterization.
They also said that a different engineered enzyme for breaking down DNA or RNA, called DNase I-XT, works better to remove residual DNA at all locations.
The authors closed by raising a series of questions that they argued must be investigated.
They asked why regulators don’t mandate other and better tests for DNA contamination, given that more comprehensive methods exist. They called for a “comprehensive reassessment of current DNA quantitation standards and manufacturing controls for modRNA-LNP therapeutics.”
They said it was concerning that regulators required multi-target PCR testing for COVID-19 tests to avoid false negatives. But they accept single-target assays for vaccine quality control — a contrast they say warrants scrutiny.
They called for an investigation into the decision to switch from Process 1 to Process 2, “given these biological products were mandated in many jurisdictions — often liability free — and reached billions of people, the attention to quality control and GMPs must exceed the standards of pharmaceuticals targeting a subset of people. These products were administered universally to the elderly, infirm, pregnant women and infants.”
Heliobas Disciple
TB Fanatic
(fair use applies)
Breaking- Deadly Mystery Disease Ravages Cuba - Authorities Conceal Shocking Truth Behind Epidemic
James Josh
Jan 13, 2026
In a chilling development that has sent shockwaves through the global health community, Cuba is grappling with an unprecedented outbreak of a mysterious disease that experts warn is unlike anything seen before. Far from the official narrative of mosquito-borne viruses like chikungunya or Oropouche..neither is it the H3N2 Flu strain, this insidious pathogen is leaving hospitals overwhelmed, morgues overflowing, and entire communities in terror. Various media outlets are trying to uncover the horrifying details that Cuban authorities are desperately trying to bury.
In this Medical News report, we delve into eyewitness accounts and sources form media and X accounts suggesting the regime is falsifying death certificates and silencing medics to downplay the crisis. Sources close to the ground reveal that what started as isolated cases in Matanzas province has exploded nationwide, infecting potentially one-third of Cuba's 9.7 million population. But here's the twist: lab tests from fleeing Cubans analyzed abroad point to a novel bacterial or viral hybrid, possibly exacerbated by contaminated water supplies and economic collapse – not the arboviruses the government claims.
Horrifying Symptoms That Defy Explanation
Victims describe an onslaught of symptoms that begin innocuously but escalate into nightmarish torment. It starts with sky-high fevers reaching 40°C (104°F), accompanied by delirium and fainting spells that leave sufferers bedridden for days. Then comes the rash: angry red spots that spread like wildfire across the skin, evolving into grotesque peeling and blistering that resembles severe chemical burns. Joints swell to agonizing proportions, rendering movement impossible – imagine your knees and elbows ballooning like overripe fruit, throbbing with pain that no painkiller can touch. But it doesn't stop there. Gastrointestinal havoc ensues with relentless vomiting and diarrhea, leading to acute dehydration that claims lives before victims can reach help. Abdominal agony mimics appendicitis, while liver inflammation hints at deeper organ damage. Neurological effects are emerging too: headaches that feel like skull-crushing vices, confusion, and in rare cases, seizures. Unlike chikungunya's typical joint pain or Oropouche's flu-like malaise, this mystery affliction lingers for weeks, with relapses that drain the life from even the healthiest individuals.
Children and the elderly are hit hardest, with reports of young lives snuffed out in hours due to rapid organ failure.
Government Cover-Up: Silenced Medics and Falsified Data
Insiders allege a deliberate concealment by Cuban authorities, who attribute the surge to known viruses to avoid international scrutiny. Leaked memos suggest officials are underreporting deaths – official tallies hover at just 33, but independent estimates put the toll in the hundreds, if not thousands. Hospitals in Havana and Matanzas are at breaking point, with bodies piling up in corridors and power outages halting life-saving equipment. Medics are threatened with arrest for speaking out, while fore ign aid is rejected to maintain the facade of a "medical powerhouse."
The economic crisis fuels the fire: garbage mountains breed unknown vectors, water shortages spread contamination, and medicine shortages leave patients to self-medicate with futile home remedies. Is this a bioweapon gone awry, a mutated superbug from neglected labs, or a consequence of regime negligence?
Many are demanding answers, as the world watches Cuba teeter on the edge of collapse.
Global Implications: Travel Warnings and Looming Pandemic Threat
As cases spill over – with infected travelers carrying the mystery pathogen to Florida and Europe – health agencies like the CDC have issued Level 2 alerts, but they too parrot the "chikungunya" line. Yet, analyses from Spain and the US reveal bacterial elements absent in standard arboviruses, raising fears of antibiotic resistance or something else. If unchecked, this could spark a hemispheric pandemic, exploiting porous borders and climate change.
Cuba's silence is deafening, but the truth is emerging through brave whistleblowers. The regime's grip tightens as protests brew amid blackouts and starvation, but the mystery disease may be the spark that ignites revolution.
Sources and Links Discussing the Mysterious Outbreak
For further reading, here are links to media outlets and X accounts reporting on the "mysterious" aspects of Cuba's health crisis:
Media Outlets:
www.the-sun.com
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
‘We are dying’: Cuba sinks into a health crisis amid medicine shortages and misdiagnosis
Cuba battling infectious disease ‘surge,’ Canadian travellers advised to take precautions
https://www.bmj.com/content/391/bmj.r2688
Cuba reports 1st chikungunya deaths in November
X Accounts:
https://x.com/outbreakupdates/status/2010709982635843938
https://x.com/MayraDo57466678/status/1973507880767856990
https://x.com/MayraDo57466678/status/1996032100969927131
https://x.com/Recon1_ZA/status/2010768069778424023
Breaking- Deadly Mystery Disease Ravages Cuba - Authorities Conceal Shocking Truth Behind Epidemic
James Josh
Jan 13, 2026
In a chilling development that has sent shockwaves through the global health community, Cuba is grappling with an unprecedented outbreak of a mysterious disease that experts warn is unlike anything seen before. Far from the official narrative of mosquito-borne viruses like chikungunya or Oropouche..neither is it the H3N2 Flu strain, this insidious pathogen is leaving hospitals overwhelmed, morgues overflowing, and entire communities in terror. Various media outlets are trying to uncover the horrifying details that Cuban authorities are desperately trying to bury.
In this Medical News report, we delve into eyewitness accounts and sources form media and X accounts suggesting the regime is falsifying death certificates and silencing medics to downplay the crisis. Sources close to the ground reveal that what started as isolated cases in Matanzas province has exploded nationwide, infecting potentially one-third of Cuba's 9.7 million population. But here's the twist: lab tests from fleeing Cubans analyzed abroad point to a novel bacterial or viral hybrid, possibly exacerbated by contaminated water supplies and economic collapse – not the arboviruses the government claims.
Horrifying Symptoms That Defy Explanation
Victims describe an onslaught of symptoms that begin innocuously but escalate into nightmarish torment. It starts with sky-high fevers reaching 40°C (104°F), accompanied by delirium and fainting spells that leave sufferers bedridden for days. Then comes the rash: angry red spots that spread like wildfire across the skin, evolving into grotesque peeling and blistering that resembles severe chemical burns. Joints swell to agonizing proportions, rendering movement impossible – imagine your knees and elbows ballooning like overripe fruit, throbbing with pain that no painkiller can touch. But it doesn't stop there. Gastrointestinal havoc ensues with relentless vomiting and diarrhea, leading to acute dehydration that claims lives before victims can reach help. Abdominal agony mimics appendicitis, while liver inflammation hints at deeper organ damage. Neurological effects are emerging too: headaches that feel like skull-crushing vices, confusion, and in rare cases, seizures. Unlike chikungunya's typical joint pain or Oropouche's flu-like malaise, this mystery affliction lingers for weeks, with relapses that drain the life from even the healthiest individuals.
Children and the elderly are hit hardest, with reports of young lives snuffed out in hours due to rapid organ failure.
Government Cover-Up: Silenced Medics and Falsified Data
Insiders allege a deliberate concealment by Cuban authorities, who attribute the surge to known viruses to avoid international scrutiny. Leaked memos suggest officials are underreporting deaths – official tallies hover at just 33, but independent estimates put the toll in the hundreds, if not thousands. Hospitals in Havana and Matanzas are at breaking point, with bodies piling up in corridors and power outages halting life-saving equipment. Medics are threatened with arrest for speaking out, while fore ign aid is rejected to maintain the facade of a "medical powerhouse."
The economic crisis fuels the fire: garbage mountains breed unknown vectors, water shortages spread contamination, and medicine shortages leave patients to self-medicate with futile home remedies. Is this a bioweapon gone awry, a mutated superbug from neglected labs, or a consequence of regime negligence?
Many are demanding answers, as the world watches Cuba teeter on the edge of collapse.
Global Implications: Travel Warnings and Looming Pandemic Threat
As cases spill over – with infected travelers carrying the mystery pathogen to Florida and Europe – health agencies like the CDC have issued Level 2 alerts, but they too parrot the "chikungunya" line. Yet, analyses from Spain and the US reveal bacterial elements absent in standard arboviruses, raising fears of antibiotic resistance or something else. If unchecked, this could spark a hemispheric pandemic, exploiting porous borders and climate change.
Cuba's silence is deafening, but the truth is emerging through brave whistleblowers. The regime's grip tightens as protests brew amid blackouts and starvation, but the mystery disease may be the spark that ignites revolution.
Sources and Links Discussing the Mysterious Outbreak
For further reading, here are links to media outlets and X accounts reporting on the "mysterious" aspects of Cuba's health crisis:
Media Outlets:
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
CUBA has been overwhelmed by a disease known as “the virus” – leaving hospitals on the verge of collapse as the Communist regime faces accusations of a cover-up. High fevers, red …
www.the-sun.com
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
‘We are dying’: Cuba sinks into a health crisis amid medicine shortages and misdiagnosis
Cuba battling infectious disease ‘surge,’ Canadian travellers advised to take precautions
https://www.bmj.com/content/391/bmj.r2688
Cuba reports 1st chikungunya deaths in November
X Accounts:
https://x.com/outbreakupdates/status/2010709982635843938
https://x.com/MayraDo57466678/status/1973507880767856990
https://x.com/MayraDo57466678/status/1996032100969927131
https://x.com/Recon1_ZA/status/2010768069778424023
Heliobas Disciple
TB Fanatic
(fair use applies)
The Amino Acid D-Alanine Shows Promise Against Flu And COVID-19
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 07, 2026
Medical News: Tiny Molecule Turns Heads in Virus Research
A growing body of science suggests a humble nutrient found in food and produced by gut bacteria could become a helping hand in fights against dangerous viral infections. New research from the National Institutes of Biomedical Innovation Health and Nutrition Japan (NIBIOHN), Tsukuba Primate Research Center, and Osaka University Graduate School of Medicine has uncovered the importance of D-alanine, a naturally occurring D-amino acid, during influenza and COVID-19 illness.
According to the study, dangerously ill mice and critically hospitalized COVID-19 patients showed a sharp drop in blood levels of several D-amino acids. Levels of D-alanine fell the hardest. When scientists added D-alanine back, infected animals tended to fare better, gaining more protection from lung injury, weight loss, and death.
What Are D-Amino Acids
Most amino acids in the body are L-forms, the molecular shape living organisms typically use. The less familiar D-forms are present in tiny amounts, often overlooked until recently. They come from the diet, gut microbes, and normal metabolism, and emerging research links them to disease detection and immune balance.
This Medical News report highlights that in severe viral illness, D-alanine levels plunge dramatically below normal—even lower than their usual lowest point in the daily sleep–wake cycle, as confirmed in multiple measurements in both mice and humans.
Key Findings from The Study
-D-alanine levels collapse during severe infection
In flu-infected mice, D-alanine dropped by more than 80 percent. Patients with life-threatening COVID-19 on ventilators or ECMO had blood D-alanine levels less than half those of healthy people.
-Lower D-alanine linked to poorer survival
Across several mouse models, the animals that lost body weight fastest and died earliest were the ones whose D-alanine never rebounded.
-Supplementation brought measurable benefit
When researchers supplied D-alanine through drinking water or injection:
*Mice lost less weight
*Their lungs showed fewer blocked air sacs, less bleeding, and reduced immune cell overrun
*Viral load in the lungs was lower
*Survival improved modestly, especially in animals that maintained higher D-alanine levels
These patterns appeared in both influenza A and SARS-CoV-2 infection experiments.
Why It Matters
D-alanine is inexpensive, found naturally in foods, and generally regarded as safe. The scientists caution that benefits were inconsistent and sometimes small because severe infection appears t o burn through D-alanine faster than supplementation can replace it. Even so, it provides two valuable tools:
-A biomarker to spot who is getting dangerously worse
-A potential supportive nutrient to soften the impact of disease while doctors use other therapies
Conclusion
This research suggests that watching D-alanine could help doctors quickly identify which patients are at highest risk from COVID-19 or influenza, and offering supplemental D-alanine—once doses and timing are refined—may improve outcomes. While the findings still need larger human trials, the study opens a promising doorway by showing that tiny metabolic clues in the blood can guide care, and everyday molecules might provide unexpected protection when viral infections strike hard.
The study findings were published in the peer reviewed journal: BBA Molecular Basis of Disease
The Amino Acid D-Alanine Shows Promise Against Flu And COVID-19
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 07, 2026
Medical News: Tiny Molecule Turns Heads in Virus Research
A growing body of science suggests a humble nutrient found in food and produced by gut bacteria could become a helping hand in fights against dangerous viral infections. New research from the National Institutes of Biomedical Innovation Health and Nutrition Japan (NIBIOHN), Tsukuba Primate Research Center, and Osaka University Graduate School of Medicine has uncovered the importance of D-alanine, a naturally occurring D-amino acid, during influenza and COVID-19 illness.
According to the study, dangerously ill mice and critically hospitalized COVID-19 patients showed a sharp drop in blood levels of several D-amino acids. Levels of D-alanine fell the hardest. When scientists added D-alanine back, infected animals tended to fare better, gaining more protection from lung injury, weight loss, and death.
What Are D-Amino Acids
Most amino acids in the body are L-forms, the molecular shape living organisms typically use. The less familiar D-forms are present in tiny amounts, often overlooked until recently. They come from the diet, gut microbes, and normal metabolism, and emerging research links them to disease detection and immune balance.
This Medical News report highlights that in severe viral illness, D-alanine levels plunge dramatically below normal—even lower than their usual lowest point in the daily sleep–wake cycle, as confirmed in multiple measurements in both mice and humans.
Key Findings from The Study
-D-alanine levels collapse during severe infection
In flu-infected mice, D-alanine dropped by more than 80 percent. Patients with life-threatening COVID-19 on ventilators or ECMO had blood D-alanine levels less than half those of healthy people.
-Lower D-alanine linked to poorer survival
Across several mouse models, the animals that lost body weight fastest and died earliest were the ones whose D-alanine never rebounded.
-Supplementation brought measurable benefit
When researchers supplied D-alanine through drinking water or injection:
*Mice lost less weight
*Their lungs showed fewer blocked air sacs, less bleeding, and reduced immune cell overrun
*Viral load in the lungs was lower
*Survival improved modestly, especially in animals that maintained higher D-alanine levels
These patterns appeared in both influenza A and SARS-CoV-2 infection experiments.
Why It Matters
D-alanine is inexpensive, found naturally in foods, and generally regarded as safe. The scientists caution that benefits were inconsistent and sometimes small because severe infection appears t o burn through D-alanine faster than supplementation can replace it. Even so, it provides two valuable tools:
-A biomarker to spot who is getting dangerously worse
-A potential supportive nutrient to soften the impact of disease while doctors use other therapies
Conclusion
This research suggests that watching D-alanine could help doctors quickly identify which patients are at highest risk from COVID-19 or influenza, and offering supplemental D-alanine—once doses and timing are refined—may improve outcomes. While the findings still need larger human trials, the study opens a promising doorway by showing that tiny metabolic clues in the blood can guide care, and everyday molecules might provide unexpected protection when viral infections strike hard.
The study findings were published in the peer reviewed journal: BBA Molecular Basis of Disease
psychgirl
TB Fanatic
WTH???(fair use applies)
Breaking- Deadly Mystery Disease Ravages Cuba - Authorities Conceal Shocking Truth Behind Epidemic
James Josh
Jan 13, 2026
In a chilling development that has sent shockwaves through the global health community, Cuba is grappling with an unprecedented outbreak of a mysterious disease that experts warn is unlike anything seen before. Far from the official narrative of mosquito-borne viruses like chikungunya or Oropouche..neither is it the H3N2 Flu strain, this insidious pathogen is leaving hospitals overwhelmed, morgues overflowing, and entire communities in terror. Various media outlets are trying to uncover the horrifying details that Cuban authorities are desperately trying to bury.
In this Medical News report, we delve into eyewitness accounts and sources form media and X accounts suggesting the regime is falsifying death certificates and silencing medics to downplay the crisis. Sources close to the ground reveal that what started as isolated cases in Matanzas province has exploded nationwide, infecting potentially one-third of Cuba's 9.7 million population. But here's the twist: lab tests from fleeing Cubans analyzed abroad point to a novel bacterial or viral hybrid, possibly exacerbated by contaminated water supplies and economic collapse – not the arboviruses the government claims.
Horrifying Symptoms That Defy Explanation
Victims describe an onslaught of symptoms that begin innocuously but escalate into nightmarish torment. It starts with sky-high fevers reaching 40°C (104°F), accompanied by delirium and fainting spells that leave sufferers bedridden for days. Then comes the rash: angry red spots that spread like wildfire across the skin, evolving into grotesque peeling and blistering that resembles severe chemical burns. Joints swell to agonizing proportions, rendering movement impossible – imagine your knees and elbows ballooning like overripe fruit, throbbing with pain that no painkiller can touch. But it doesn't stop there. Gastrointestinal havoc ensues with relentless vomiting and diarrhea, leading to acute dehydration that claims lives before victims can reach help. Abdominal agony mimics appendicitis, while liver inflammation hints at deeper organ damage. Neurological effects are emerging too: headaches that feel like skull-crushing vices, confusion, and in rare cases, seizures. Unlike chikungunya's typical joint pain or Oropouche's flu-like malaise, this mystery affliction lingers for weeks, with relapses that drain the life from even the healthiest individuals.
Children and the elderly are hit hardest, with reports of young lives snuffed out in hours due to rapid organ failure.
Government Cover-Up: Silenced Medics and Falsified Data
Insiders allege a deliberate concealment by Cuban authorities, who attribute the surge to known viruses to avoid international scrutiny. Leaked memos suggest officials are underreporting deaths – official tallies hover at just 33, but independent estimates put the toll in the hundreds, if not thousands. Hospitals in Havana and Matanzas are at breaking point, with bodies piling up in corridors and power outages halting life-saving equipment. Medics are threatened with arrest for speaking out, while fore ign aid is rejected to maintain the facade of a "medical powerhouse."
The economic crisis fuels the fire: garbage mountains breed unknown vectors, water shortages spread contamination, and medicine shortages leave patients to self-medicate with futile home remedies. Is this a bioweapon gone awry, a mutated superbug from neglected labs, or a consequence of regime negligence?
Many are demanding answers, as the world watches Cuba teeter on the edge of collapse.
Global Implications: Travel Warnings and Looming Pandemic Threat
As cases spill over – with infected travelers carrying the mystery pathogen to Florida and Europe – health agencies like the CDC have issued Level 2 alerts, but they too parrot the "chikungunya" line. Yet, analyses from Spain and the US reveal bacterial elements absent in standard arboviruses, raising fears of antibiotic resistance or something else. If unchecked, this could spark a hemispheric pandemic, exploiting porous borders and climate change.
Cuba's silence is deafening, but the truth is emerging through brave whistleblowers. The regime's grip tightens as protests brew amid blackouts and starvation, but the mystery disease may be the spark that ignites revolution.
Sources and Links Discussing the Mysterious Outbreak
For further reading, here are links to media outlets and X accounts reporting on the "mysterious" aspects of Cuba's health crisis:
Media Outlets:
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
CUBA has been overwhelmed by a disease known as “the virus” – leaving hospitals on the verge of collapse as the Communist regime faces accusations of a cover-up. High fevers, red …
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
‘We are dying’: Cuba sinks into a health crisis amid medicine shortages and misdiagnosis
Cuba battling infectious disease ‘surge,’ Canadian travellers advised to take precautions
https://www.bmj.com/content/391/bmj.r2688
Cuba reports 1st chikungunya deaths in November
X Accounts:
https://x.com/outbreakupdates/status/2010709982635843938
https://x.com/MayraDo57466678/status/1973507880767856990
https://x.com/MayraDo57466678/status/1996032100969927131
https://x.com/Recon1_ZA/status/2010768069778424023
Is this real??
Heliobas Disciple
TB Fanatic
WTH???
Is this real??
I don't know. I clicked on all his links, looks like this has been going on in Cuba since at least October. It reminded me of how COVID came about, cases started the fall before (1999) but it wasn't really reported on until January of the next year (2020). And because I trust Nik at TMN, I thought if he's alarmed, it's worth posting. Not worth it's own thread yet, because it seems like very little info is out there at this point, but worth reporting to those of us who follow Nik on this thread.
HD
Heliobas Disciple
TB Fanatic
The manuscript he links to is really long and hard to format. Last time it took me over 20 minutes to bring over and multiple posts, so this time I am just leaving the link for you to click on if you want to try to read it there. It's pretty techinical. bottom line, he's not backing down from his prediction. (see the text I bolded below).
voiceforscienceandsolidarity.substack.com
(fair use applies) BOLDING MINE
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape.
Dismissing alternative evolutionary trajectories for SARS-CoV-2 because they are uncomfortable or unprecedented does not reflect scientific consensus....
Geert Vanden Bossche
Jan 14, 2026
I am hesitant to share my latest manuscript:
Note to readers:
Some of my followers may raise their eyebrows at reading this article and think I'm schizophrenic for sharing such complex (and mostly incomprehensible ??) analysis of the COVID-19 pandemic. However, my main goal is to thoroughly document my insights and the science behind it. That way, no so-called global health expert, authority, or anyone else who pushed the mass vaccination can ever claim the pandemic's disastrous outcome was totally unpredictable or unrelated to the mass vaccination program.
Even though I personally believe AI will eventually become a plague to humanity (probably sooner than we think), it's still in a constructive and positively impactful phase for now. I, therefore, recommend that anyone who gives me even a shred of credibility ask any AI tool to verify my theory, and even simplify and explain the message in my last article, and also my previous one (From Enhanced Infectiousness to Enhanced Virulence: Why a Glycosylation-Driven Shift in SARS-CoV-2 Evolution Has Become Increasingly Likely) in plain language. That would add substantial value to this comprehensive analysis as it would credibly warn the widest possible audience about the impending HI-VI-CRON tsunami.
In the meantime, I can only advise all those primed by COVID vaccines to prophylactically start taking a safe and effective antiviral treatment at the very first sign of this tsunami (IMO, most clearly signaled by a sudden and sharp surge in hyperacute disease and mortality in one or more highly C-19-vaccinated regions) and to continue it until the tsunami has completely passed.
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape.
Dismissing alternative evolutionary trajectories for SARS-CoV-2 because they are uncomfortable or unprecedented does not reflect scientific consensus....
voiceforscienceandsolidarity.substack.com
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape.
Dismissing alternative evolutionary trajectories for SARS-CoV-2 because they are uncomfortable or unprecedented does not reflect scientific consensus....
Geert Vanden Bossche
Jan 14, 2026
I am hesitant to share my latest manuscript:
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape
The absence of worsening clinical signals during the emergence of newly circulating variants does not imply intrinsic attenuation of SARS-CoV-2 (SC-2) or its transition toward endemicity but instead sets the stage for the selection of additional, virulence-enabling O-glycosylation as last-resort...
www.trialsitenews.com
Note to readers:
Some of my followers may raise their eyebrows at reading this article and think I'm schizophrenic for sharing such complex (and mostly incomprehensible ??) analysis of the COVID-19 pandemic. However, my main goal is to thoroughly document my insights and the science behind it. That way, no so-called global health expert, authority, or anyone else who pushed the mass vaccination can ever claim the pandemic's disastrous outcome was totally unpredictable or unrelated to the mass vaccination program.
Even though I personally believe AI will eventually become a plague to humanity (probably sooner than we think), it's still in a constructive and positively impactful phase for now. I, therefore, recommend that anyone who gives me even a shred of credibility ask any AI tool to verify my theory, and even simplify and explain the message in my last article, and also my previous one (From Enhanced Infectiousness to Enhanced Virulence: Why a Glycosylation-Driven Shift in SARS-CoV-2 Evolution Has Become Increasingly Likely) in plain language. That would add substantial value to this comprehensive analysis as it would credibly warn the widest possible audience about the impending HI-VI-CRON tsunami.
In the meantime, I can only advise all those primed by COVID vaccines to prophylactically start taking a safe and effective antiviral treatment at the very first sign of this tsunami (IMO, most clearly signaled by a sudden and sharp surge in hyperacute disease and mortality in one or more highly C-19-vaccinated regions) and to continue it until the tsunami has completely passed.
Heliobas Disciple
TB Fanatic
(fair use applies)
RED LARGE TEXT IS MINE - because it goes back to Geert's theory in the post above this.
ALSO REMEMBER NOT TO GIVE ASPIRIN TO CHILDREN BECAUSE OF THE RISK OF REYE'S SYNDROME.
Italian Researchers Discover That Aspirin Disrupts COVID-19 Spike Protein Before It Harms the Body
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 08, 2026
Medical News: Aspirin’s Surprising New Ability Revealed
Researchers from Istituto di Ricerche Farmacologiche Mario Negri IRCCS in Bergamo Italy have made an unexpected discovery about aspirin. Long known for easing pain and reducing inflammation, aspirin also appears to directly interfere with the SARS-CoV-2 spike protein’s ability to attach to the human ACE2 receptor. This brand-new finding suggests aspirin may weaken the very first step of viral attack, offering a potential new role for one of the world’s most common medicines.
How the virus normally gains entry
The SARS-CoV-2 coronavirus spike protein uses its S1 portion to latch onto ACE2, a receptor found throughout the lungs, heart, blood vessels, kidneys and brain. This attachment opens the door for infection and can trigger inflammation, clotting, tissue injury and long-term symptoms. Even in patients no longer carrying active virus, circulating spike fragments can still cause harm.
Aspirin weakens spike binding in the lab
In the new study, scientists mixed purified spike S1 protein with different concentrations of aspirin before introducing it to living cells. They found that aspirin-treated spike bound far less successfully to ACE2. The effect strengthened with higher aspirin levels, showing a clear dose-dependent pattern. The same treatment using paracetamol showed no benefit, confirming that aspirin’s effect was unique.
Animal testing strengthens the evidence
To see whether this effect mattered in living tissue, the team tested aspirin-treated spike protein in mice engineered to express human ACE2. Animals exposed to untreated spike developed swollen lung tissue, heavy inflammatory cell infiltration and early fibrotic scarring. In contrast, mice that received spike pre-treated with aspirin showed dramatically reduced lung injury, little collagen buildup and far fewer immune cells.
Importantly, giving aspirin after the spike exposure offered no protection. This proves that aspirin must interact with the spike protein itself before it reaches the body, rather than acting through its usual anti-inflammatory pathways.
The key breakthrough: aspirin alters spike sugar structures
The study’s most important discovery was that aspirin changes the spike protein’s glycosylation—the sugary coating that helps the virus bind ACE2 and avoid the immune system. Aspirin removed or altered sugars at several locations, especially at N61 and S325. When researchers created spike proteins lacking those exact sugar sites, the mutants behaved just like aspirin-modified spike: they barely attached to ACE2 and caused only mild lung abnormalities in mice.
This shows that disrupting spike glycosylation is the major reason aspirin reduces its harmful activity.
Why this matters
This Medical News report highlights a potential new use for a cheap, globally available medication. If further research confirms these results in humans, aspirin could become part of an early intervention strategy to weaken the spike protein before it drives tissue damage or long COVID-related complications. Although more clinical research is needed, this discovery provides a promising new angle for reducing the severity of SARS-CoV-2 infection using a familiar and low-cost drug.
The study findings were published in the peer reviewed journal: Frontiers in Immunology.
www.frontiersin.org
RED LARGE TEXT IS MINE - because it goes back to Geert's theory in the post above this.
ALSO REMEMBER NOT TO GIVE ASPIRIN TO CHILDREN BECAUSE OF THE RISK OF REYE'S SYNDROME.
Italian Researchers Discover That Aspirin Disrupts COVID-19 Spike Protein Before It Harms the Body
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 08, 2026
Medical News: Aspirin’s Surprising New Ability Revealed
Researchers from Istituto di Ricerche Farmacologiche Mario Negri IRCCS in Bergamo Italy have made an unexpected discovery about aspirin. Long known for easing pain and reducing inflammation, aspirin also appears to directly interfere with the SARS-CoV-2 spike protein’s ability to attach to the human ACE2 receptor. This brand-new finding suggests aspirin may weaken the very first step of viral attack, offering a potential new role for one of the world’s most common medicines.
How the virus normally gains entry
The SARS-CoV-2 coronavirus spike protein uses its S1 portion to latch onto ACE2, a receptor found throughout the lungs, heart, blood vessels, kidneys and brain. This attachment opens the door for infection and can trigger inflammation, clotting, tissue injury and long-term symptoms. Even in patients no longer carrying active virus, circulating spike fragments can still cause harm.
Aspirin weakens spike binding in the lab
In the new study, scientists mixed purified spike S1 protein with different concentrations of aspirin before introducing it to living cells. They found that aspirin-treated spike bound far less successfully to ACE2. The effect strengthened with higher aspirin levels, showing a clear dose-dependent pattern. The same treatment using paracetamol showed no benefit, confirming that aspirin’s effect was unique.
Animal testing strengthens the evidence
To see whether this effect mattered in living tissue, the team tested aspirin-treated spike protein in mice engineered to express human ACE2. Animals exposed to untreated spike developed swollen lung tissue, heavy inflammatory cell infiltration and early fibrotic scarring. In contrast, mice that received spike pre-treated with aspirin showed dramatically reduced lung injury, little collagen buildup and far fewer immune cells.
Importantly, giving aspirin after the spike exposure offered no protection. This proves that aspirin must interact with the spike protein itself before it reaches the body, rather than acting through its usual anti-inflammatory pathways.
The key breakthrough: aspirin alters spike sugar structures
The study’s most important discovery was that aspirin changes the spike protein’s glycosylation—the sugary coating that helps the virus bind ACE2 and avoid the immune system. Aspirin removed or altered sugars at several locations, especially at N61 and S325. When researchers created spike proteins lacking those exact sugar sites, the mutants behaved just like aspirin-modified spike: they barely attached to ACE2 and caused only mild lung abnormalities in mice.
This shows that disrupting spike glycosylation is the major reason aspirin reduces its harmful activity.
Why this matters
This Medical News report highlights a potential new use for a cheap, globally available medication. If further research confirms these results in humans, aspirin could become part of an early intervention strategy to weaken the spike protein before it drives tissue damage or long COVID-related complications. Although more clinical research is needed, this discovery provides a promising new angle for reducing the severity of SARS-CoV-2 infection using a familiar and low-cost drug.
The study findings were published in the peer reviewed journal: Frontiers in Immunology.
Frontiers | Acetylsalicylic acid disrupts SARS-CoV-2 spike protein glycosylation and selectively impairs binding to ACE2
Preclinical and clinical evidence suggested the potential benefits of treatment with acetylsalicylic acid (ASA) in mitigating COVID-19 severity. While availa...
www.frontiersin.org
Weft and Warp
Senior Member
This part of that paper makes no sense at all:
" Importantly, giving aspirin after the spike exposure offered no protection. This proves that aspirin must interact with the spike protein itself before it reaches the body, rather than acting through its usual anti-inflammatory pathways."
Unless, they mean to say that the aspirin needs to be in the body before getting exposed and not after? A person would have to take aspirin everyday if that was the case because you can't predict when you'll get exposed. I guess we're going back to the "baby aspirin" every day stuff.
" Importantly, giving aspirin after the spike exposure offered no protection. This proves that aspirin must interact with the spike protein itself before it reaches the body, rather than acting through its usual anti-inflammatory pathways."
Unless, they mean to say that the aspirin needs to be in the body before getting exposed and not after? A person would have to take aspirin everyday if that was the case because you can't predict when you'll get exposed. I guess we're going back to the "baby aspirin" every day stuff.
Zoner
Veteran Member
Thanks for doing this HD. He really is NOT backing off his prediction. It's been years now trying to understand his technical reasonings and his many failed timing forecasts. I've timed out on him. I guess it doesn't really matter if you're not vaxxed and if you are you're doomed according to Geert. According to him it can't be stopped so might as well just keep on praying.The manuscript he links to is really long and hard to format. Last time it took me over 20 minutes to bring over and multiple posts, so this time I am just leaving the link for you to click on if you want to try to read it there. It's pretty techinical. bottom line, he's not backing down from his prediction. (see the text I bolded below).
(fair use applies) BOLDING MINEPlausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape.
Dismissing alternative evolutionary trajectories for SARS-CoV-2 because they are uncomfortable or unprecedented does not reflect scientific consensus....
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape.
Dismissing alternative evolutionary trajectories for SARS-CoV-2 because they are uncomfortable or unprecedented does not reflect scientific consensus....
Geert Vanden Bossche
Jan 14, 2026
I am hesitant to share my latest manuscript:
Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape
The absence of worsening clinical signals during the emergence of newly circulating variants does not imply intrinsic attenuation of SARS-CoV-2 (SC-2) or its transition toward endemicity but instead sets the stage for the selection of additional, virulence-enabling O-glycosylation as last-resort...www.trialsitenews.com
Note to readers:
Some of my followers may raise their eyebrows at reading this article and think I'm schizophrenic for sharing such complex (and mostly incomprehensible ??) analysis of the COVID-19 pandemic. However, my main goal is to thoroughly document my insights and the science behind it. That way, no so-called global health expert, authority, or anyone else who pushed the mass vaccination can ever claim the pandemic's disastrous outcome was totally unpredictable or unrelated to the mass vaccination program.
Even though I personally believe AI will eventually become a plague to humanity (probably sooner than we think), it's still in a constructive and positively impactful phase for now. I, therefore, recommend that anyone who gives me even a shred of credibility ask any AI tool to verify my theory, and even simplify and explain the message in my last article, and also my previous one (From Enhanced Infectiousness to Enhanced Virulence: Why a Glycosylation-Driven Shift in SARS-CoV-2 Evolution Has Become Increasingly Likely) in plain language. That would add substantial value to this comprehensive analysis as it would credibly warn the widest possible audience about the impending HI-VI-CRON tsunami.
In the meantime, I can only advise all those primed by COVID vaccines to prophylactically start taking a safe and effective antiviral treatment at the very first sign of this tsunami (IMO, most clearly signaled by a sudden and sharp surge in hyperacute disease and mortality in one or more highly C-19-vaccinated regions) and to continue it until the tsunami has completely passed.
Old Greek
Veteran Member
Been doing that for 40 years!
psychgirl
TB Fanatic
I’d fallen off the GVB page too for a bit.
But then he started posting again and I believe him.
None of this is going away
March 3rd, 1 year date from when I had my heart attack, I come off of clopidogrel for (stents) and start daily aspirin. Sounds like that will be a good thing.
Still no Afib so probably cutting eliquis dosage in half as well.
Countrymouse
Country exile in the city
Dear God--please keep this away from the USA!(fair use applies)
Breaking- Deadly Mystery Disease Ravages Cuba - Authorities Conceal Shocking Truth Behind Epidemic
James Josh
Jan 13, 2026
In a chilling development that has sent shockwaves through the global health community, Cuba is grappling with an unprecedented outbreak of a mysterious disease that experts warn is unlike anything seen before. Far from the official narrative of mosquito-borne viruses like chikungunya or Oropouche..neither is it the H3N2 Flu strain, this insidious pathogen is leaving hospitals overwhelmed, morgues overflowing, and entire communities in terror. Various media outlets are trying to uncover the horrifying details that Cuban authorities are desperately trying to bury.
In this Medical News report, we delve into eyewitness accounts and sources form media and X accounts suggesting the regime is falsifying death certificates and silencing medics to downplay the crisis. Sources close to the ground reveal that what started as isolated cases in Matanzas province has exploded nationwide, infecting potentially one-third of Cuba's 9.7 million population. But here's the twist: lab tests from fleeing Cubans analyzed abroad point to a novel bacterial or viral hybrid, possibly exacerbated by contaminated water supplies and economic collapse – not the arboviruses the government claims.
Horrifying Symptoms That Defy Explanation
Victims describe an onslaught of symptoms that begin innocuously but escalate into nightmarish torment. It starts with sky-high fevers reaching 40°C (104°F), accompanied by delirium and fainting spells that leave sufferers bedridden for days. Then comes the rash: angry red spots that spread like wildfire across the skin, evolving into grotesque peeling and blistering that resembles severe chemical burns. Joints swell to agonizing proportions, rendering movement impossible – imagine your knees and elbows ballooning like overripe fruit, throbbing with pain that no painkiller can touch. But it doesn't stop there. Gastrointestinal havoc ensues with relentless vomiting and diarrhea, leading to acute dehydration that claims lives before victims can reach help. Abdominal agony mimics appendicitis, while liver inflammation hints at deeper organ damage. Neurological effects are emerging too: headaches that feel like skull-crushing vices, confusion, and in rare cases, seizures. Unlike chikungunya's typical joint pain or Oropouche's flu-like malaise, this mystery affliction lingers for weeks, with relapses that drain the life from even the healthiest individuals.
Children and the elderly are hit hardest, with reports of young lives snuffed out in hours due to rapid organ failure.
Government Cover-Up: Silenced Medics and Falsified Data
Insiders allege a deliberate concealment by Cuban authorities, who attribute the surge to known viruses to avoid international scrutiny. Leaked memos suggest officials are underreporting deaths – official tallies hover at just 33, but independent estimates put the toll in the hundreds, if not thousands. Hospitals in Havana and Matanzas are at breaking point, with bodies piling up in corridors and power outages halting life-saving equipment. Medics are threatened with arrest for speaking out, while fore ign aid is rejected to maintain the facade of a "medical powerhouse."
The economic crisis fuels the fire: garbage mountains breed unknown vectors, water shortages spread contamination, and medicine shortages leave patients to self-medicate with futile home remedies. Is this a bioweapon gone awry, a mutated superbug from neglected labs, or a consequence of regime negligence?
Many are demanding answers, as the world watches Cuba teeter on the edge of collapse.
Global Implications: Travel Warnings and Looming Pandemic Threat
As cases spill over – with infected travelers carrying the mystery pathogen to Florida and Europe – health agencies like the CDC have issued Level 2 alerts, but they too parrot the "chikungunya" line. Yet, analyses from Spain and the US reveal bacterial elements absent in standard arboviruses, raising fears of antibiotic resistance or something else. If unchecked, this could spark a hemispheric pandemic, exploiting porous borders and climate change.
Cuba's silence is deafening, but the truth is emerging through brave whistleblowers. The regime's grip tightens as protests brew amid blackouts and starvation, but the mystery disease may be the spark that ignites revolution.
Sources and Links Discussing the Mysterious Outbreak
For further reading, here are links to media outlets and X accounts reporting on the "mysterious" aspects of Cuba's health crisis:
Media Outlets:
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
CUBA has been overwhelmed by a disease known as “the virus” – leaving hospitals on the verge of collapse as the Communist regime faces accusations of a cover-up. High fevers, red …
'Mystery virus' leaves Cuba hospitals on verge of collapse as medics 'silenced'
‘We are dying’: Cuba sinks into a health crisis amid medicine shortages and misdiagnosis
Cuba battling infectious disease ‘surge,’ Canadian travellers advised to take precautions
https://www.bmj.com/content/391/bmj.r2688
Cuba reports 1st chikungunya deaths in November
X Accounts:
https://x.com/outbreakupdates/status/2010709982635843938
https://x.com/MayraDo57466678/status/1973507880767856990
https://x.com/MayraDo57466678/status/1996032100969927131
https://x.com/Recon1_ZA/status/2010768069778424023
psychgirl
TB Fanatic
Amen to that!!
Heliobas Disciple
TB Fanatic
I agree. I think this is just preliminary, I'm not sure taking it prophylactically would work either since it had to be on the spike before the body encounters it. If I had to guess, I'm going to think they may come out with a safe nasal spray or throat spray that encounters the spike before it gets to the lungs is how this would work and what someone should be working on creating. SEE MY ETA's BELOW - never inhale aspirin, it can kill you. They would have to come up with a safe way to make it a nasal spray, this is not a do-it-yourself option. In the meantime though a baby aspirin a day has other benefits so if you can take it (no bleeding problems, ulcers, not a child, etc) that may help ???? I don't know. Interesting study though and I hope someone follows up with how to use that knowledge to help people.
Btw, if the "Geert variant" should show up, I think we should think of creative ways to use aspirin in our every day lives before covid gets in our bodies. Maybe crush and dissolve it in water and spray down counters, wipe down door knobs, etc. Soak your clothes, towels, sheets, etc in aspirin water before doing the wash? And how much aspirin would you need? I really don't know but information like this seems to be something to keep in the back burner should an emergency come up and we're desperate to keep covid out of our bodies...
ETA: I am definitely not advocating spraying your nose with aspirin water. That seems really dangerous to me. I think it's too risky and could bring all sorts of other problems for your sinuses and maybe even your brain. I would never do it, even if the "Geert Variant" was around. Although I might dissolve aspirin and soak a mask in it and wear the dried mask if I was desperate, as long as I wasn't inhaling any aspirin dust. An aspirin mask... omg...that sounds so insane ! I hope we never get to a situation where I'd be so desperate to even consider something so outrageous.
ETA2: I was right, just googled it. DO NOT INHALE ASPIRIN. it could kill you. Definitely defeats the purpose!
HD
Last edited:
Heliobas Disciple
TB Fanatic
(fair use applies)
SARS-CoV-2 is on the decline in animals, researchers find
by Meg Dalton, Yale University
edited by Gaby Clark, reviewed by Robert Egan
January 9, 2026
During the first few years of the COVID-19 pandemic, the virus SARS-CoV-2 was detected in an increasing number of non-human animal species. This included many wild animal species as well as domestic animals such as dogs and cats.
In some animals, like the white-tailed deer and mink, scientists found that the virus spread readily within the species, and then, with newly acquired mutations, spilled back into the human population. This sparked concern that a parallel evolution of SARS-CoV-2 in animals could create a more transmissible or pathogenic variant that could reignite a surge in human infection.
So where do things stand today? In a new study, Yale researchers investigated just that. They conducted surveillance studies to understand the current coronaviral landscape of wild and domestic animals in the northeastern United States. They found that while SARS-CoV-2 continues evolving in humans, its grip on the animal kingdom seems to be weakening.
"This is good news as this reduces the chance of spillback of newly evolved animal variants into humans," said Caroline Zeiss, professor of comparative medicine and of ophthalmology and visual science at Yale School of Medicine (YSM) and senior author of the new study.
She added, "Ongoing monitoring is essential, particularly for viruses that are capable of infecting many species, such as corona and influenza viruses. Long-term surveillance of wildlife and animals living close to humans gives us a unique chance to spot new pathogens that might spread to humans or affect animal health."
The study appears in the journal Scientific Reports.
Surveilling viruses
Coronaviruses can have a very broad host range and jump across animal species. This ability was at the root of the SARS CoV-2 virus crossing the animal-human boundary to trigger the COVID-19 pandemic, scientists say.
Since its emergence, SARS-CoV-2 has undergone rapid evolution, with one variant succeeding another as the virus became increasingly transmissible in its predominant human host. This progression has been accompanied by evidence for human-to-animal transmission of circulating variants, as well as sustained transmission within certain species like the white-tailed deer.
Rates of SARS-CoV-2 prevalence or infection in animal samples have declined since the peak of the pandemic. But it's been unclear whether that reflects an actual decline in rates or reduced resources for surveillance studies.
For the new study, the researchers wanted to get closer to understanding just that. So, they conducted a broad surveillance study of SARS-CoV-2 in wild and domestic animal species in the northeastern U.S., including cats, dogs, ferrets, woodchucks, cattle, and more. They collected fecal swabs, oral swabs, or stool specimens from 889 animals. Collection of these samples was a collaborative effort between the Connecticut Veterinary Medical Diagnostic Laboratory at the University of Connecticut, the Connecticut Agricultural Experiment Station, and Yale University.
Samples were analyzed for coronaviral RNA using an assay method that is able to detect a broad range of coronavirus types. Positive samples were then sequenced to identify the coronavirus species within the sample. In addition, researchers conducted a genetic analysis of most of the positive samples to provide independent verification of their results.
To complement the surveillance study, they conducted experimental infections of white-footed mice in the laboratory using the original strain of SARS-CoV-2 and the more recent omicron variant. They focused on white-footed mice as they are the most common wild rodents in the area. They also have a known role in the spread of pathogens between humans and other animals like the white-tailed deer.
And, to test cross-species transmission, they exposed hamsters—which are known to be a very good and susceptible model of SARS-CoV-2 infection—to contaminated bedding and cages from the mice infected with SARS-CoV-2.
"Our goal was to determine whether both variants could infect white-footed mice and whether they could transmit the virus to each another or to another species," Zeiss said.
Protecting our pets
Through both the surveillance and lab studies, the researchers detected several kinds of animal coronaviruses in samples from seven different species, though none of them had SARS-CoV-2. When they infected the white-footed mice with SARS-CoV-2, the mice could catch both the original and omicron variants, though they didn't shed as much of the virus with the omicron variant and did not transmit it between them.
Importantly, the original strain could spread among the mice, but neither the original nor the omicron version could jump to another species like hamsters.
Taken together, researchers say, the findings suggest that as SARS-CoV-2 continues evolving in its preferred host (humans), successive variants may be losing their affinity for non-human animals.
"Therefore, the chance of spillback of newly evolved animal variants into humans is very low," Zeiss said. "For most people, this is relevant to pet owners who live in close contact with animals."
Publication details
Sylvester Ibemgbo et al, The coronaviral landscape across diverse mammalian species in the Northeastern United States, Scientific Reports (2025). DOI: 10.1038/s41598-025-32849-3
Journal information: Scientific Reports
Key medical concepts
SARS-CoV-2Coronavirus
Clinical categories
Infectious diseasesCommon illnesses & Prevention
Provided by Yale University
SARS-CoV-2 is on the decline in animals, researchers find
by Meg Dalton, Yale University
edited by Gaby Clark, reviewed by Robert Egan
January 9, 2026
During the first few years of the COVID-19 pandemic, the virus SARS-CoV-2 was detected in an increasing number of non-human animal species. This included many wild animal species as well as domestic animals such as dogs and cats.
In some animals, like the white-tailed deer and mink, scientists found that the virus spread readily within the species, and then, with newly acquired mutations, spilled back into the human population. This sparked concern that a parallel evolution of SARS-CoV-2 in animals could create a more transmissible or pathogenic variant that could reignite a surge in human infection.
So where do things stand today? In a new study, Yale researchers investigated just that. They conducted surveillance studies to understand the current coronaviral landscape of wild and domestic animals in the northeastern United States. They found that while SARS-CoV-2 continues evolving in humans, its grip on the animal kingdom seems to be weakening.
"This is good news as this reduces the chance of spillback of newly evolved animal variants into humans," said Caroline Zeiss, professor of comparative medicine and of ophthalmology and visual science at Yale School of Medicine (YSM) and senior author of the new study.
She added, "Ongoing monitoring is essential, particularly for viruses that are capable of infecting many species, such as corona and influenza viruses. Long-term surveillance of wildlife and animals living close to humans gives us a unique chance to spot new pathogens that might spread to humans or affect animal health."
The study appears in the journal Scientific Reports.
Surveilling viruses
Coronaviruses can have a very broad host range and jump across animal species. This ability was at the root of the SARS CoV-2 virus crossing the animal-human boundary to trigger the COVID-19 pandemic, scientists say.
Since its emergence, SARS-CoV-2 has undergone rapid evolution, with one variant succeeding another as the virus became increasingly transmissible in its predominant human host. This progression has been accompanied by evidence for human-to-animal transmission of circulating variants, as well as sustained transmission within certain species like the white-tailed deer.
Rates of SARS-CoV-2 prevalence or infection in animal samples have declined since the peak of the pandemic. But it's been unclear whether that reflects an actual decline in rates or reduced resources for surveillance studies.
For the new study, the researchers wanted to get closer to understanding just that. So, they conducted a broad surveillance study of SARS-CoV-2 in wild and domestic animal species in the northeastern U.S., including cats, dogs, ferrets, woodchucks, cattle, and more. They collected fecal swabs, oral swabs, or stool specimens from 889 animals. Collection of these samples was a collaborative effort between the Connecticut Veterinary Medical Diagnostic Laboratory at the University of Connecticut, the Connecticut Agricultural Experiment Station, and Yale University.
Samples were analyzed for coronaviral RNA using an assay method that is able to detect a broad range of coronavirus types. Positive samples were then sequenced to identify the coronavirus species within the sample. In addition, researchers conducted a genetic analysis of most of the positive samples to provide independent verification of their results.
To complement the surveillance study, they conducted experimental infections of white-footed mice in the laboratory using the original strain of SARS-CoV-2 and the more recent omicron variant. They focused on white-footed mice as they are the most common wild rodents in the area. They also have a known role in the spread of pathogens between humans and other animals like the white-tailed deer.
And, to test cross-species transmission, they exposed hamsters—which are known to be a very good and susceptible model of SARS-CoV-2 infection—to contaminated bedding and cages from the mice infected with SARS-CoV-2.
"Our goal was to determine whether both variants could infect white-footed mice and whether they could transmit the virus to each another or to another species," Zeiss said.
Protecting our pets
Through both the surveillance and lab studies, the researchers detected several kinds of animal coronaviruses in samples from seven different species, though none of them had SARS-CoV-2. When they infected the white-footed mice with SARS-CoV-2, the mice could catch both the original and omicron variants, though they didn't shed as much of the virus with the omicron variant and did not transmit it between them.
Importantly, the original strain could spread among the mice, but neither the original nor the omicron version could jump to another species like hamsters.
Taken together, researchers say, the findings suggest that as SARS-CoV-2 continues evolving in its preferred host (humans), successive variants may be losing their affinity for non-human animals.
"Therefore, the chance of spillback of newly evolved animal variants into humans is very low," Zeiss said. "For most people, this is relevant to pet owners who live in close contact with animals."
Publication details
Sylvester Ibemgbo et al, The coronaviral landscape across diverse mammalian species in the Northeastern United States, Scientific Reports (2025). DOI: 10.1038/s41598-025-32849-3
Journal information: Scientific Reports
Key medical concepts
SARS-CoV-2Coronavirus
Clinical categories
Infectious diseasesCommon illnesses & Prevention
Provided by Yale University
Heliobas Disciple
TB Fanatic
(fair use applies)
Nitric Oxide Nasal Spray Shows Potential Against Influenza Virus, SARS-CoV-2 Variants and Major Respiratory Viruses
Nikhil Prasad Fact checked by:Thailand Medical New Team
Jan 12, 2026
Medical News: A New Tool Against Everyday Lung Infections
A new laboratory investigation led by scientists from SaNOtize Research & Development Corp. in Vancouver, Canada, together with experts from the Department of Pathology and Laboratory Medicine at the University of British Columbia and Respiratory Medicine at the University of British Columbia, has revealed highly promising results showing that a Nitric Oxide Nasal Spray (NONS) can rapidly neutralize a wide range of dangerous respiratory viruses. This Medical News report describes how the simple nose spray may offer everyday protection against viruses responsible for colds, flu, and even COVID-19.
Why Researchers Tested the Spray
Respiratory viruses spread mainly from the nose and throat, where they first multiply after entering the body. Many of these viruses, including influenza, RSV, and SARS-CoV-2, mutate quickly and can become resistant to medicines or vaccines. Some, like human rhinovirus and certain influenza strains, have no reliable treatments at all. With repeated COVID-19 waves and resurging flu threats, researchers believe that a broad-acting antiviral that works directly inside the nose could slow infections before they spread deeper into the body.
Testing Nitric Oxide on a Long List of Threats
The study exposed viruses to the nasal spray in controlled experiments and measured how much active virus remained after short contact times ranging from 5 seconds to 2 minutes. The researchers reported that NONS eliminated more than 99.9 percent of infectious virus across many targets, often bringing viral levels down to undetectable limits.
Key findings include:
• All major SARS-CoV-2 variants, including Alpha, Delta, Omicron BA.1 and XBB.2, were wiped out within 30 seconds to two minutes
• Influenza A (H1N1, H3N2, H5N1) and Influenza B were among the easiest to kill, disappearing in 10–15 seconds
• Respiratory syncytial virus, human metapneumovirus, and parainfluenza virus type 3 were eliminated within two minutes
• Even human rhinovirus, a hard-to-kill virus linked to the common cold, was neutralized to below detectable levels
The antiviral effect comes from nitric oxide, a natural immune molecule that interferes with the viral structures they need to infect human cells.
Why This Matters for Public Health
While vaccines and medicines remain essential, experts stress that viruses continue to evolve faster than drug development timelines. Because NONS works by directly damaging the virus instead of targeting a specific variant, it may stay effective even when new strains emerge. The spray is self-administered, acts locally in the nose, and has shown a strong safety profile in earlier clinical studies.
Conclusions
The new findings suggest that Nitric Oxide Nasal Spray may serve as a practical, rapid-acting antiviral option in homes, schools, travel settings and healthcare facilities. By sharply reducing viral levels in the nose—the place infections begin—it could lower the chances of serious sickness and transmission, even against novel or vaccine-resistant strains. Researchers emphasize that future clinical trials will confirm how well this benefit translates into real-world protection, but the laboratory results already show a broad and fast-acting antiviral approach that strengthens pandemic preparedness and everyday respiratory defense.
The study findings were published in the peer reviewed journal: Viruses
Nitric Oxide Nasal Spray Shows Potential Against Influenza Virus, SARS-CoV-2 Variants and Major Respiratory Viruses
Nikhil Prasad Fact checked by:Thailand Medical New Team
Jan 12, 2026
Medical News: A New Tool Against Everyday Lung Infections
A new laboratory investigation led by scientists from SaNOtize Research & Development Corp. in Vancouver, Canada, together with experts from the Department of Pathology and Laboratory Medicine at the University of British Columbia and Respiratory Medicine at the University of British Columbia, has revealed highly promising results showing that a Nitric Oxide Nasal Spray (NONS) can rapidly neutralize a wide range of dangerous respiratory viruses. This Medical News report describes how the simple nose spray may offer everyday protection against viruses responsible for colds, flu, and even COVID-19.
Why Researchers Tested the Spray
Respiratory viruses spread mainly from the nose and throat, where they first multiply after entering the body. Many of these viruses, including influenza, RSV, and SARS-CoV-2, mutate quickly and can become resistant to medicines or vaccines. Some, like human rhinovirus and certain influenza strains, have no reliable treatments at all. With repeated COVID-19 waves and resurging flu threats, researchers believe that a broad-acting antiviral that works directly inside the nose could slow infections before they spread deeper into the body.
Testing Nitric Oxide on a Long List of Threats
The study exposed viruses to the nasal spray in controlled experiments and measured how much active virus remained after short contact times ranging from 5 seconds to 2 minutes. The researchers reported that NONS eliminated more than 99.9 percent of infectious virus across many targets, often bringing viral levels down to undetectable limits.
Key findings include:
• All major SARS-CoV-2 variants, including Alpha, Delta, Omicron BA.1 and XBB.2, were wiped out within 30 seconds to two minutes
• Influenza A (H1N1, H3N2, H5N1) and Influenza B were among the easiest to kill, disappearing in 10–15 seconds
• Respiratory syncytial virus, human metapneumovirus, and parainfluenza virus type 3 were eliminated within two minutes
• Even human rhinovirus, a hard-to-kill virus linked to the common cold, was neutralized to below detectable levels
The antiviral effect comes from nitric oxide, a natural immune molecule that interferes with the viral structures they need to infect human cells.
Why This Matters for Public Health
While vaccines and medicines remain essential, experts stress that viruses continue to evolve faster than drug development timelines. Because NONS works by directly damaging the virus instead of targeting a specific variant, it may stay effective even when new strains emerge. The spray is self-administered, acts locally in the nose, and has shown a strong safety profile in earlier clinical studies.
Conclusions
The new findings suggest that Nitric Oxide Nasal Spray may serve as a practical, rapid-acting antiviral option in homes, schools, travel settings and healthcare facilities. By sharply reducing viral levels in the nose—the place infections begin—it could lower the chances of serious sickness and transmission, even against novel or vaccine-resistant strains. Researchers emphasize that future clinical trials will confirm how well this benefit translates into real-world protection, but the laboratory results already show a broad and fast-acting antiviral approach that strengthens pandemic preparedness and everyday respiratory defense.
The study findings were published in the peer reviewed journal: Viruses
psychgirl
TB Fanatic
Heliobas Disciple
TB Fanatic
(fair use applies)
COVID-19 Devastates the Thymus, Sparking an Immune Crisis in Many
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 13, 2026
In the shadowy depths of our immune system lies a small but mighty organ called the thymus, often overlooked until now. As the world grapples with the lingering shadows of the COVID-19 pandemic, groundbreaking research reveals a chilling truth: the SARS-CoV-2 virus doesn't just ravage the lungs—it launches a stealth attack on the thymus, crippling our body's defense headquarters and setting the stage for long-haul health nightmares. This Medical News report dives deep into how this insidious virus turns the thymus dysfunctional, why it matters, and the ripple effects that could haunt survivors for years.
The Vital Role of the Thymus in Our Immune Arsenal
Tucked behind the breastbone, the thymus is no mere bystander in the body's fight against invaders. This butterfly-shaped gland is the boot camp for T-cells, those elite warriors of the adaptive immune system. From birth, it takes immature cells from the bone marrow and molds them into sophisticated fighters capable of recognizing and destroying specific threats like viruses, bacteria, and even cancer cells. The thymus ensures T-cells learn to distinguish friend from foe through a rigorous selection process: positive selection hones their ability to spot foreign antigens, while negative selection weeds out those that might attack the body's own tissues, preventing autoimmune chaos.
Peak performance hits in childhood, but by adulthood, the thymus begins to shrink—a natural process called involution. Yet, it never fully retires, continuing to churn out fresh, naïve T cells that replenish our immune repertoire. Without a healthy thymus, we'd be left with a stagnant army of aging T-cells, vulnerable to new pathogens and prone to misfires. It's the unsung hero keeping our immunity diverse, responsive, and balanced.
SARS-CoV-2's Sneak Attack on the Thymus
Enter SARS-CoV-2, the crafty coronavirus behind COVID-19. Studies show this virus doesn't stop at the respiratory tract; it infiltrates the thymus directly, hijacking its cells and sparking a cascade of destruction. Researchers have found viral particles in thymic tissue, where the virus infects thymocytes—the precursors to T-cells—and epithelial cells that nurture them. This invasion triggers massive inflammation, apoptosis (programmed cell death), and atrophy, shrinking the organ and halting its output.
One pivotal study using autopsy samples and patient data revealed that COVID-19 patients exhibit reduced thymic function, directly correlating with disease severity. In severe cases, the thymus shows altered gene expression, with upregulated inflammatory pathways and downregulated genes crucial for T-cell maturation.
Mouse models infected with SARS-CoV-2 variants like Delta demonstrated severe thymic atrophy, marked by a drastic drop in double-positive (CD4+CD8+) T-cells—up to 80% loss in some instances—driven by interferon-gam ma (IFN-?) signaling.
This cytokine storm not only kills off developing T-cells but also disrupts the thymic microenvironment, leading to fibrosis and long-term scarring.
Even milder variants like Omicron cause marginal atrophy, but the original strains and Delta wreak havoc, depleting the T-cell pipeline. In fetal infections, SARS-CoV-2 reaches the thymus via intraamniotic routes, causing DNA damage and immune imbalance, as seen in elevated markers like HMGB1 and CD86.
Genetic factors play a role too; polymorphisms in the TCRA-TCRD locus, which influence thymic output, determine how robustly the immune system rebounds post-infection.
Health Fallout from a Compromised Thymus
When SARS-CoV-2 sabotages the thymus, the consequences echo far beyond acute illness. A dysfunctional thymus means fewer new T-cells entering circulation, resulting in a narrowed T-cell receptor (TCR) repertoire. This "immune exhaustion" leaves patients susceptible to secondary infections, from bacterial pneumonia to opportunistic fungi.
Long COVID sufferers often report persistent fatigue, brain fog, and autoimmune flares—symptoms linked to this thymic hit. Studies tie thymic involution to inflammaging, where chronic low-grade inflammation accelerates aging and boosts risks for conditions like diabetes, heart disease, and even cancer.
In elderly patients, already dealing with age-related thymic shrinkage, COVID-19 exacerbates the problem, leading to "acute T-cell exhaustion." This isn't just peripheral; it's central, disrupting the thymus's oversight of immune homeostasis. Research shows that boosting thymic output with thymosin alpha-1 (Ta1) in severe cases restores T-cell counts, reduces mortality by up to 50%, and cuts reliance on ventilators. Without intervention, survivors face waning immunity, poorer vaccine responses, and a higher autoimmune disease incidence, as self-reactive T cells slip through unchecked.
Detailed Insights from Groundbreaking Studies
Delving into specifics, a 2023 study in the Journal of Allergy and Clinical Immunology examined 200 COVID-19 patients and found thymic epithelial cells expressing ACE2 receptors—the virus's entry point—making them prime targets.
Infected thymi displayed a 40-60% reduction in recent thymic emigrants (RTEs), correlating with ICU stays and mortality rates exceeding 30% in severe groups. Autopsies revealed viral RNA in 70% of thymic samples from deceased patients, with histological changes including lymphoid depletion and hemorrhage.
Another investigation using K18-hACE2 transgenic mice highlighted variant-specific effects: Delta infection caused near-total depletion of double-positive T cells within days, mediated by IFN-?, as neutralizing antibodies against it reversed atrophy. Remdesivir treatment not only curbed lung viral loads but also preserved thymic structure, restoring T-cell maturation pathways. In humans, CT scans of 465 adults showed pneumonia 3.85 times more prevalent in those without visible thymus, with infected lung segments averaging 4.84 times higher.
Fetal studies detected high viral loads in the thymus, leading to proteomic shifts with upregulated DNA damage responses and immune markers, potentially stunting lifelong immunity. Genetic analyses linked the rs2204985 GG genotype to better thymic reactivation, higher naïve T-cell counts, and milder pneumonia, underscoring personalized risks.
These revelations paint a dire picture, yet they offer hope through targeted therapies. By understanding SARS-CoV-2's thymic assault, we can develop interventions like thymic peptides or antivirals to shield this vital organ, potentially mitigating long-term immune woes and enhancing recovery. The pandemic's hidden toll on the thymus reminds us that COVID-19's legacy extends deep into our biology, urging vigilance and innovation in post-viral care.
As we reflect on these findings, the implications are profound: SARS-CoV-2's targeting of the thymus not only amplifies acute disease severity but also seeds chronic immune dysregulation, heightening vulnerability to infections, autoimmunity, and age-related ailments. Boosting thymic function through drugs like Ta1 or antivirals could revolutionize treatment, offering a lifeline to restore T-cell diversity and resilience. This underscores the need for ongoing research to combat the virus's long shadow on global health, potentially saving countless lives by fortifying our inner defenses against future threats.
References:
https://onlinelibrary.wiley.com/doi/full/10.1002/eji.202350624
https://www.mdpi.com/2073-4409/10/3/628
https://www.science.org/doi/10.1126/sciadv.adh7969
Evaluation of the relationship between the presence of thymus gland and COVID-19 pneumonia in adult patients
Presence of SARS-CoV-2 in fetal organs via intraamniotic infection - Nature Communications
Frontiers | Immune damage mechanisms of COVID-19 and novel strategies in prevention and control of epidemic
https://www.mdpi.com/2076-393X/9/10/1119
Europe PMC
COVID-19 infects the thymus and impairs the immune system
https://www.sciencedirect.com/science/article/pii/S2589004223000494
COVID-19 Devastates the Thymus, Sparking an Immune Crisis in Many
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 13, 2026
In the shadowy depths of our immune system lies a small but mighty organ called the thymus, often overlooked until now. As the world grapples with the lingering shadows of the COVID-19 pandemic, groundbreaking research reveals a chilling truth: the SARS-CoV-2 virus doesn't just ravage the lungs—it launches a stealth attack on the thymus, crippling our body's defense headquarters and setting the stage for long-haul health nightmares. This Medical News report dives deep into how this insidious virus turns the thymus dysfunctional, why it matters, and the ripple effects that could haunt survivors for years.
The Vital Role of the Thymus in Our Immune Arsenal
Tucked behind the breastbone, the thymus is no mere bystander in the body's fight against invaders. This butterfly-shaped gland is the boot camp for T-cells, those elite warriors of the adaptive immune system. From birth, it takes immature cells from the bone marrow and molds them into sophisticated fighters capable of recognizing and destroying specific threats like viruses, bacteria, and even cancer cells. The thymus ensures T-cells learn to distinguish friend from foe through a rigorous selection process: positive selection hones their ability to spot foreign antigens, while negative selection weeds out those that might attack the body's own tissues, preventing autoimmune chaos.
Peak performance hits in childhood, but by adulthood, the thymus begins to shrink—a natural process called involution. Yet, it never fully retires, continuing to churn out fresh, naïve T cells that replenish our immune repertoire. Without a healthy thymus, we'd be left with a stagnant army of aging T-cells, vulnerable to new pathogens and prone to misfires. It's the unsung hero keeping our immunity diverse, responsive, and balanced.
SARS-CoV-2's Sneak Attack on the Thymus
Enter SARS-CoV-2, the crafty coronavirus behind COVID-19. Studies show this virus doesn't stop at the respiratory tract; it infiltrates the thymus directly, hijacking its cells and sparking a cascade of destruction. Researchers have found viral particles in thymic tissue, where the virus infects thymocytes—the precursors to T-cells—and epithelial cells that nurture them. This invasion triggers massive inflammation, apoptosis (programmed cell death), and atrophy, shrinking the organ and halting its output.
One pivotal study using autopsy samples and patient data revealed that COVID-19 patients exhibit reduced thymic function, directly correlating with disease severity. In severe cases, the thymus shows altered gene expression, with upregulated inflammatory pathways and downregulated genes crucial for T-cell maturation.
Mouse models infected with SARS-CoV-2 variants like Delta demonstrated severe thymic atrophy, marked by a drastic drop in double-positive (CD4+CD8+) T-cells—up to 80% loss in some instances—driven by interferon-gam ma (IFN-?) signaling.
This cytokine storm not only kills off developing T-cells but also disrupts the thymic microenvironment, leading to fibrosis and long-term scarring.
Even milder variants like Omicron cause marginal atrophy, but the original strains and Delta wreak havoc, depleting the T-cell pipeline. In fetal infections, SARS-CoV-2 reaches the thymus via intraamniotic routes, causing DNA damage and immune imbalance, as seen in elevated markers like HMGB1 and CD86.
Genetic factors play a role too; polymorphisms in the TCRA-TCRD locus, which influence thymic output, determine how robustly the immune system rebounds post-infection.
Health Fallout from a Compromised Thymus
When SARS-CoV-2 sabotages the thymus, the consequences echo far beyond acute illness. A dysfunctional thymus means fewer new T-cells entering circulation, resulting in a narrowed T-cell receptor (TCR) repertoire. This "immune exhaustion" leaves patients susceptible to secondary infections, from bacterial pneumonia to opportunistic fungi.
Long COVID sufferers often report persistent fatigue, brain fog, and autoimmune flares—symptoms linked to this thymic hit. Studies tie thymic involution to inflammaging, where chronic low-grade inflammation accelerates aging and boosts risks for conditions like diabetes, heart disease, and even cancer.
In elderly patients, already dealing with age-related thymic shrinkage, COVID-19 exacerbates the problem, leading to "acute T-cell exhaustion." This isn't just peripheral; it's central, disrupting the thymus's oversight of immune homeostasis. Research shows that boosting thymic output with thymosin alpha-1 (Ta1) in severe cases restores T-cell counts, reduces mortality by up to 50%, and cuts reliance on ventilators. Without intervention, survivors face waning immunity, poorer vaccine responses, and a higher autoimmune disease incidence, as self-reactive T cells slip through unchecked.
Detailed Insights from Groundbreaking Studies
Delving into specifics, a 2023 study in the Journal of Allergy and Clinical Immunology examined 200 COVID-19 patients and found thymic epithelial cells expressing ACE2 receptors—the virus's entry point—making them prime targets.
Infected thymi displayed a 40-60% reduction in recent thymic emigrants (RTEs), correlating with ICU stays and mortality rates exceeding 30% in severe groups. Autopsies revealed viral RNA in 70% of thymic samples from deceased patients, with histological changes including lymphoid depletion and hemorrhage.
Another investigation using K18-hACE2 transgenic mice highlighted variant-specific effects: Delta infection caused near-total depletion of double-positive T cells within days, mediated by IFN-?, as neutralizing antibodies against it reversed atrophy. Remdesivir treatment not only curbed lung viral loads but also preserved thymic structure, restoring T-cell maturation pathways. In humans, CT scans of 465 adults showed pneumonia 3.85 times more prevalent in those without visible thymus, with infected lung segments averaging 4.84 times higher.
Fetal studies detected high viral loads in the thymus, leading to proteomic shifts with upregulated DNA damage responses and immune markers, potentially stunting lifelong immunity. Genetic analyses linked the rs2204985 GG genotype to better thymic reactivation, higher naïve T-cell counts, and milder pneumonia, underscoring personalized risks.
These revelations paint a dire picture, yet they offer hope through targeted therapies. By understanding SARS-CoV-2's thymic assault, we can develop interventions like thymic peptides or antivirals to shield this vital organ, potentially mitigating long-term immune woes and enhancing recovery. The pandemic's hidden toll on the thymus reminds us that COVID-19's legacy extends deep into our biology, urging vigilance and innovation in post-viral care.
As we reflect on these findings, the implications are profound: SARS-CoV-2's targeting of the thymus not only amplifies acute disease severity but also seeds chronic immune dysregulation, heightening vulnerability to infections, autoimmunity, and age-related ailments. Boosting thymic function through drugs like Ta1 or antivirals could revolutionize treatment, offering a lifeline to restore T-cell diversity and resilience. This underscores the need for ongoing research to combat the virus's long shadow on global health, potentially saving countless lives by fortifying our inner defenses against future threats.
References:
https://onlinelibrary.wiley.com/doi/full/10.1002/eji.202350624
https://www.mdpi.com/2073-4409/10/3/628
https://www.science.org/doi/10.1126/sciadv.adh7969
Evaluation of the relationship between the presence of thymus gland and COVID-19 pneumonia in adult patients
Presence of SARS-CoV-2 in fetal organs via intraamniotic infection - Nature Communications
Frontiers | Immune damage mechanisms of COVID-19 and novel strategies in prevention and control of epidemic
https://www.mdpi.com/2076-393X/9/10/1119
Europe PMC
COVID-19 infects the thymus and impairs the immune system
https://www.sciencedirect.com/science/article/pii/S2589004223000494
Heliobas Disciple
TB Fanatic
Just reporting what's in the news with this one..... because I can't figure out who they were polling... ymmv
(fair use applies)
Most COVID-19 vaccine hesitancy linked to concerns that can be overcome, study suggests
by Lancet
edited by Sadie Harley, reviewed by Robert Egan
January 12, 2026
Most COVID-19 vaccine hesitancy is rooted in concerns that can be addressed and effectively reduced over time, according to a new study following more than 1.1 million people in England between January 2021 and March 2022 during the COVID-19 pandemic, published in The Lancet.
The study, led by researchers from Imperial College London, found that of the participants initially hesitant about getting a COVID-19 vaccine, 65% went on to get vaccinated at least once.
The findings offer a novel perspective on the main types of vaccine hesitancy during the COVID-19 pandemic. Their potential to be reversed may help inform the targeting and messaging for future roll-outs of novel vaccines.
While vaccine hesitancy is not a new phenomenon, with WHO naming vaccine hesitancy as one of the top 10 global health threats in 2019, reduced uptake of various vaccines, including childhood vaccinations against measles and pertussis (whooping cough), remains a major public health concern.
COVID-19 vaccination roll-out began in the UK on 8th December 2020, with a phased strategy that prioritized vaccines on the basis of age and clinical need.
"We wanted to look at COVID-19 vaccine hesitancy in more depth to identify groups with more persistent forms of hesitancy and their main concerns. Understanding these drivers is critical to address vaccine uptake and better control disease spread," explained lead author Professor Marc Chadeau-Hyam from Imperial College London, UK.
Researchers analyzed longitudinal survey data from 1.1 million adults (aged 18 and older, 57% female) from the Real-time Assessment of Community Transmission (REACT) Study (at the time of the initial COVID-19 vaccine roll-out between January 2021 and March 2022). They compared vaccine attitudes at enrollment with subsequent vaccination uptake from National Health Service (NHS) vaccination records up to May 7, 2024, to identify categories and drivers of vaccine hesitancy.
During the pandemic, participants were asked whether they had been or intended to get vaccinated. Those who refused the vaccine, or were skeptical about vaccination, were asked about their reasons for hesitancy from a checklist of 23 options as well as a free text option.
Vaccine effectiveness and health effects key reasons for hesitancy
Overall, 3.3% (37,982 of 1.1 million) of participants reported some degree of COVID-19 vaccine hesitancy and subsequent vaccination data were available through NHS records linkage for 24,229 (64%) of them.
Hesitancy rates declined over time from an initial high of 8% of those surveyed in January 2021, to a low of 1.1% at the start of 2022. There was a small uptick in hesitancy to over 2.2% in February and March 2022 during the omicron wave.
The researchers identified eight categories of vaccine hesitancy, including concerns about effectiveness and side effects, perception of low risk from COVID-19 and mistrust of vaccine developers, and fear of vaccines and reactions.
Among the hesitant who provided a reason for hesitancy, 41% (12,498 of 30,701) reported concerns around long-term health effects, 39% (11,953) that they wanted to wait to see whether the vaccine worked, and 37% (11,287) that they had concerns about side effects.
Reasons for hesitancy varied across demographic groups, with, for example, men more likely than women to report not feeling COVID-19 was a personal risk (18% vs. 10%); women more likely to be worried about fertility-related consequences (21% vs. 8%), while those aged 74 years or older were more likely to be against vaccines in general compared with 18–24 year olds (12% vs. 2.5%).
The analysis of subsequent vaccination behavior found that the likelihood of remaining unvaccinated was higher for older people, women, people of Black ethnicity, people who were unemployed or living in deprived areas, those with a history of COVID-19, and people with a lower level of education.
Majority of vaccine-hesitant individuals got vaccinated
People who reported the most common reasons for hesitancy (i.e., those related to vaccine efficacy or health concerns), were most likely to change their mind and subsequently get vaccinated against COVID-19.
In contrast, people expressing hesitancy relating to lack of trust, perception of low personal risk, and general anti-vaccine sentiment were two to three-times less likely to get vaccinated compared to those who did not report these reasons.
"We show that certain types of vaccine hesitancy are more readily addressed than others, for example, concerns relating to pregnancy or breastfeeding," said co-author Professor Helen Ward from Imperial College London and the National Institute for Health and Care Research Imperial Biomedical Research Center, UK.
"Our study suggests that as the vaccine was rolled out, public confidence increased and the original vaccine skepticism was largely overcome."
According to co-author Professor Paul Elliott from Imperial College London, "What we learned from the COVID-19 experience is the importance of ensuring that people have access to reliable and trusted information so they can make well-informed decisions about their personal health choices.
"Reliable, easy-to-understand information, for example, on vaccine effectiveness and potential risks, is of particular importance in the case of a public health emergency such as COVID-19, which involved the rapid deployment at-scale of new vaccine technologies."
The authors acknowledge some limitations of the study, including that NHS vaccine records and self-reported vaccine status showed some inconsistencies, likely reflecting both imperfect recall and imperfect coverage in the NHS data. Additionally, vaccine hesitant respondents were less likely to consent to NHS record linkage, potentially introducing selection bias, which may limit the generalizability of the findings.
Writing in a linked Comment, Professor Silvio Tafuri from the University of Bari Aldo Moro, Bari, Italy (who was not involved with the study) underscored the "valuable contribution" of the study and concluded, "whereas these data reflect the extraordinary setting of SARS-CoV-2 vaccination, it is crucial to ascertain whether similar drivers of hesitancy affect ordinary (ie, routine or seasonal) vaccinations, in order to guide context-specific public health interventions at the micro, meso, and macro levels."
Publication details
Profiling vaccine attitudes and subsequent uptake in 1·1 million people in England: a nationwide cohort study, The Lancet (2026). DOI: 10.1016/S0140-6736(25)01912-9
Journal information: The Lancet
Key medical concepts
Vaccination HesitancyCOVID-19 VaccineMeaslesPertussis Vaccine
Clinical categories
Preventive medicineCommon illnesses & PreventionInfectious diseases
Provided by Lancet
(fair use applies)
Most COVID-19 vaccine hesitancy linked to concerns that can be overcome, study suggests
by Lancet
edited by Sadie Harley, reviewed by Robert Egan
January 12, 2026
Most COVID-19 vaccine hesitancy is rooted in concerns that can be addressed and effectively reduced over time, according to a new study following more than 1.1 million people in England between January 2021 and March 2022 during the COVID-19 pandemic, published in The Lancet.
The study, led by researchers from Imperial College London, found that of the participants initially hesitant about getting a COVID-19 vaccine, 65% went on to get vaccinated at least once.
The findings offer a novel perspective on the main types of vaccine hesitancy during the COVID-19 pandemic. Their potential to be reversed may help inform the targeting and messaging for future roll-outs of novel vaccines.
While vaccine hesitancy is not a new phenomenon, with WHO naming vaccine hesitancy as one of the top 10 global health threats in 2019, reduced uptake of various vaccines, including childhood vaccinations against measles and pertussis (whooping cough), remains a major public health concern.
COVID-19 vaccination roll-out began in the UK on 8th December 2020, with a phased strategy that prioritized vaccines on the basis of age and clinical need.
"We wanted to look at COVID-19 vaccine hesitancy in more depth to identify groups with more persistent forms of hesitancy and their main concerns. Understanding these drivers is critical to address vaccine uptake and better control disease spread," explained lead author Professor Marc Chadeau-Hyam from Imperial College London, UK.
Researchers analyzed longitudinal survey data from 1.1 million adults (aged 18 and older, 57% female) from the Real-time Assessment of Community Transmission (REACT) Study (at the time of the initial COVID-19 vaccine roll-out between January 2021 and March 2022). They compared vaccine attitudes at enrollment with subsequent vaccination uptake from National Health Service (NHS) vaccination records up to May 7, 2024, to identify categories and drivers of vaccine hesitancy.
During the pandemic, participants were asked whether they had been or intended to get vaccinated. Those who refused the vaccine, or were skeptical about vaccination, were asked about their reasons for hesitancy from a checklist of 23 options as well as a free text option.
Vaccine effectiveness and health effects key reasons for hesitancy
Overall, 3.3% (37,982 of 1.1 million) of participants reported some degree of COVID-19 vaccine hesitancy and subsequent vaccination data were available through NHS records linkage for 24,229 (64%) of them.
Hesitancy rates declined over time from an initial high of 8% of those surveyed in January 2021, to a low of 1.1% at the start of 2022. There was a small uptick in hesitancy to over 2.2% in February and March 2022 during the omicron wave.
The researchers identified eight categories of vaccine hesitancy, including concerns about effectiveness and side effects, perception of low risk from COVID-19 and mistrust of vaccine developers, and fear of vaccines and reactions.
Among the hesitant who provided a reason for hesitancy, 41% (12,498 of 30,701) reported concerns around long-term health effects, 39% (11,953) that they wanted to wait to see whether the vaccine worked, and 37% (11,287) that they had concerns about side effects.
Reasons for hesitancy varied across demographic groups, with, for example, men more likely than women to report not feeling COVID-19 was a personal risk (18% vs. 10%); women more likely to be worried about fertility-related consequences (21% vs. 8%), while those aged 74 years or older were more likely to be against vaccines in general compared with 18–24 year olds (12% vs. 2.5%).
The analysis of subsequent vaccination behavior found that the likelihood of remaining unvaccinated was higher for older people, women, people of Black ethnicity, people who were unemployed or living in deprived areas, those with a history of COVID-19, and people with a lower level of education.
Majority of vaccine-hesitant individuals got vaccinated
People who reported the most common reasons for hesitancy (i.e., those related to vaccine efficacy or health concerns), were most likely to change their mind and subsequently get vaccinated against COVID-19.
In contrast, people expressing hesitancy relating to lack of trust, perception of low personal risk, and general anti-vaccine sentiment were two to three-times less likely to get vaccinated compared to those who did not report these reasons.
"We show that certain types of vaccine hesitancy are more readily addressed than others, for example, concerns relating to pregnancy or breastfeeding," said co-author Professor Helen Ward from Imperial College London and the National Institute for Health and Care Research Imperial Biomedical Research Center, UK.
"Our study suggests that as the vaccine was rolled out, public confidence increased and the original vaccine skepticism was largely overcome."
According to co-author Professor Paul Elliott from Imperial College London, "What we learned from the COVID-19 experience is the importance of ensuring that people have access to reliable and trusted information so they can make well-informed decisions about their personal health choices.
"Reliable, easy-to-understand information, for example, on vaccine effectiveness and potential risks, is of particular importance in the case of a public health emergency such as COVID-19, which involved the rapid deployment at-scale of new vaccine technologies."
The authors acknowledge some limitations of the study, including that NHS vaccine records and self-reported vaccine status showed some inconsistencies, likely reflecting both imperfect recall and imperfect coverage in the NHS data. Additionally, vaccine hesitant respondents were less likely to consent to NHS record linkage, potentially introducing selection bias, which may limit the generalizability of the findings.
Writing in a linked Comment, Professor Silvio Tafuri from the University of Bari Aldo Moro, Bari, Italy (who was not involved with the study) underscored the "valuable contribution" of the study and concluded, "whereas these data reflect the extraordinary setting of SARS-CoV-2 vaccination, it is crucial to ascertain whether similar drivers of hesitancy affect ordinary (ie, routine or seasonal) vaccinations, in order to guide context-specific public health interventions at the micro, meso, and macro levels."
Publication details
Profiling vaccine attitudes and subsequent uptake in 1·1 million people in England: a nationwide cohort study, The Lancet (2026). DOI: 10.1016/S0140-6736(25)01912-9
Journal information: The Lancet
Key medical concepts
Vaccination HesitancyCOVID-19 VaccineMeaslesPertussis Vaccine
Clinical categories
Preventive medicineCommon illnesses & PreventionInfectious diseases
Provided by Lancet
Heliobas Disciple
TB Fanatic
(fair use applies)
Increased levels of Alzheimer's-linked protein found in some with long COVID
by Stony Brook University
edited by Sadie Harley, reviewed by Robert Egan
January 13, 2026
A study of 227 individuals who experienced neurocognitive difficulties post COVID-19 infection—such as headaches, vertigo, balance dysregulation, changes in taste/smell, and brain fog—displayed a significant increase in their blood plasma of a crucial protein called tau, which is found in nerves and especially in the brain. Excess levels of tau are linked to neurodegenerative diseases and found in many Alzheimer's patients.
Published in eBioMedicine, the study suggests that people who experience long COVID neurocognitive symptoms could be at further risk for neurodegenerative diseases.
Study details and participant groups
The research involves ongoing blood biomarker studies of 9/11 World Trade Center (WTC) responders who are monitored by clinicians and researchers at the Stony Brook WTC Health and Wellness Program. The research team analyzed plasma samples taken prior to the participants' COVID-19 infections and many months to years after having COVID-19.
They measured a specific tau protein, pTau-181, which stands for phosphorylated tau, an abnormal type associated with dementia patients.
Overall, the cohort showed a 59% increase of tau (pTau-181) in their plasma post COVID-19 infection while or after experiencing neurocognitive symptoms, compared to their plasma tau levels pre-COVID-19.
All the participants are individuals with some form of long COVID, or, specifically for this study, those with Neurological Post-Acute Sequelae COVID (N-PASC).
"The presence of tau at higher levels in the blood is a known biomarker of lasting brain damage," says Sean Clouston, Ph.D., Corresponding Author and Professor in the Department of Family, Population and Preventive Medicine in the Renaissance School of Medicine (RSOM) and Program in Public Health at Stony Brook University.
"Therefore, these study results imply that long COVID could worsen with time and cause changes in neurological symptoms or lead to cognitive difficulties that become worse. Yet, we do not know if this increase in tau in our sample represents a biological course that could be similar to individuals who develop Alzheimer's or related diseases."
The 227 individuals with N-PASC were compared to 227 other WTC responders who either 1) did not contract COVID between their pre- and post-pandemic blood sample collection dates, or 2) developed COVID but did not develop any long COVID symptoms, including neurological ones. This cohort served as the control group for the study.
Unlike those with N-PASC, any increased plasma tau levels in the control group from their pre-COVID tau levels was not evident based on testing.
Time could be an enemy
For those with N-PASC who had neurocognitive symptoms for more than 1.5 years, the tau level increases were worse. This finding, the authors write, "might portend worsened cognitive functioning as individuals age."
"We measured tau at an average of 2.2 years after COVID-19 infection, and our measurements taken ranged from six months to four years," adds Xiaohua Yang, First Author and Senior Research Program Manager at the Stony Brook WTC Health and Wellness Program.
"This sampling timeframe represents a true long-term post-acute sequela of COVID-19."
Clouston and colleagues stress that other research steps need to be taken to determine if increased plasma levels of tau in those with N-PASC have any association with cognitive decline or neurodegenerative diseases.
"One important step is to validate our study results using neuroimaging tools to see if tau plasma level increases also represent increased levels in the participants' brains," explains Clouston.
Additionally, the authors also point out that the cohort for this study—WTC responders—have also had more environmental exposures than the general population. Therefore, findings in N-PASC individuals who are WTC responders could be much different from the general patient population.
"The long-term impact of COVID-19 may be consequential years after the infection and give rise to long-term illnesses including neurocognitive problems similar to what is seen in Alzheimer's disease," says Senior Author Benjamin J. Luft, MD, Director of the WTC Health and Wellness Program, an infectious diseases specialist, and the Edmund D. Pelligrino Professor of Medicine in the RSOM.
"This is one of the first studies to show that a virus may contribute to the development of abnormal tau production over time," he adds.
"This has important implications for our understanding of the biological factors involved in the development of neurodegenerative disease. On a practical level, it has important implications for the development of effective vaccines and therapies to prevent an acute infection before it can embed itself in people and cause long-term disease."
Publication details
Xiaohua Yang et al, Increased phosphorylated tau (pTau-181) is associated with neurological post-acute sequelae of coronavirus disease in essential workers: a prospective cohort study before and after COVID-19 onset, eBioMedicine (2026). DOI: 10.1016/j.ebiom.2025.106106
Journal information: EBioMedicine
Key medical concepts
tau ProteinsTau protein.phosphorylated 181Alzheimer's Disease
Clinical categories
NeurologyInfectious diseases
Provided by Stony Brook University
Increased levels of Alzheimer's-linked protein found in some with long COVID
by Stony Brook University
edited by Sadie Harley, reviewed by Robert Egan
January 13, 2026
A study of 227 individuals who experienced neurocognitive difficulties post COVID-19 infection—such as headaches, vertigo, balance dysregulation, changes in taste/smell, and brain fog—displayed a significant increase in their blood plasma of a crucial protein called tau, which is found in nerves and especially in the brain. Excess levels of tau are linked to neurodegenerative diseases and found in many Alzheimer's patients.
Published in eBioMedicine, the study suggests that people who experience long COVID neurocognitive symptoms could be at further risk for neurodegenerative diseases.
Study details and participant groups
The research involves ongoing blood biomarker studies of 9/11 World Trade Center (WTC) responders who are monitored by clinicians and researchers at the Stony Brook WTC Health and Wellness Program. The research team analyzed plasma samples taken prior to the participants' COVID-19 infections and many months to years after having COVID-19.
They measured a specific tau protein, pTau-181, which stands for phosphorylated tau, an abnormal type associated with dementia patients.
Overall, the cohort showed a 59% increase of tau (pTau-181) in their plasma post COVID-19 infection while or after experiencing neurocognitive symptoms, compared to their plasma tau levels pre-COVID-19.
All the participants are individuals with some form of long COVID, or, specifically for this study, those with Neurological Post-Acute Sequelae COVID (N-PASC).
"The presence of tau at higher levels in the blood is a known biomarker of lasting brain damage," says Sean Clouston, Ph.D., Corresponding Author and Professor in the Department of Family, Population and Preventive Medicine in the Renaissance School of Medicine (RSOM) and Program in Public Health at Stony Brook University.
"Therefore, these study results imply that long COVID could worsen with time and cause changes in neurological symptoms or lead to cognitive difficulties that become worse. Yet, we do not know if this increase in tau in our sample represents a biological course that could be similar to individuals who develop Alzheimer's or related diseases."
The 227 individuals with N-PASC were compared to 227 other WTC responders who either 1) did not contract COVID between their pre- and post-pandemic blood sample collection dates, or 2) developed COVID but did not develop any long COVID symptoms, including neurological ones. This cohort served as the control group for the study.
Unlike those with N-PASC, any increased plasma tau levels in the control group from their pre-COVID tau levels was not evident based on testing.
Time could be an enemy
For those with N-PASC who had neurocognitive symptoms for more than 1.5 years, the tau level increases were worse. This finding, the authors write, "might portend worsened cognitive functioning as individuals age."
"We measured tau at an average of 2.2 years after COVID-19 infection, and our measurements taken ranged from six months to four years," adds Xiaohua Yang, First Author and Senior Research Program Manager at the Stony Brook WTC Health and Wellness Program.
"This sampling timeframe represents a true long-term post-acute sequela of COVID-19."
Clouston and colleagues stress that other research steps need to be taken to determine if increased plasma levels of tau in those with N-PASC have any association with cognitive decline or neurodegenerative diseases.
"One important step is to validate our study results using neuroimaging tools to see if tau plasma level increases also represent increased levels in the participants' brains," explains Clouston.
Additionally, the authors also point out that the cohort for this study—WTC responders—have also had more environmental exposures than the general population. Therefore, findings in N-PASC individuals who are WTC responders could be much different from the general patient population.
"The long-term impact of COVID-19 may be consequential years after the infection and give rise to long-term illnesses including neurocognitive problems similar to what is seen in Alzheimer's disease," says Senior Author Benjamin J. Luft, MD, Director of the WTC Health and Wellness Program, an infectious diseases specialist, and the Edmund D. Pelligrino Professor of Medicine in the RSOM.
"This is one of the first studies to show that a virus may contribute to the development of abnormal tau production over time," he adds.
"This has important implications for our understanding of the biological factors involved in the development of neurodegenerative disease. On a practical level, it has important implications for the development of effective vaccines and therapies to prevent an acute infection before it can embed itself in people and cause long-term disease."
Publication details
Xiaohua Yang et al, Increased phosphorylated tau (pTau-181) is associated with neurological post-acute sequelae of coronavirus disease in essential workers: a prospective cohort study before and after COVID-19 onset, eBioMedicine (2026). DOI: 10.1016/j.ebiom.2025.106106
Journal information: EBioMedicine
Key medical concepts
tau ProteinsTau protein.phosphorylated 181Alzheimer's Disease
Clinical categories
NeurologyInfectious diseases
Provided by Stony Brook University
Heliobas Disciple
TB Fanatic
https://www.thailandmedical.news/news/bromhexine-shows-strong-potential-against-new-covid-19-strains
(fair use applies)Bromhexine Shows Strong Potential Against New COVID-19 Strains
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 14, 2026
Medical News: A Common Cough Medicine Reveals Powerful Antiviral Activity
A new study by researchers from Universidad de Talca, Universidad Católica del Maule, Universidad de Concepción, and the Center for Nanomedicine ND3 and CEDENNA has uncovered surprising antiviral power in bromhexine, a widely used cough medication. According to this Medical News report, the drug appears to significantly reduce the ability of SARS-CoV-2 Omicron and other variants to infect human cells, offering fresh hope for low-cost therapies that work even as the virus evolves.
How the Researchers Tested Bromhexine
Scientists used a specially engineered human cell line called HEK293ACE2, which carries the ACE2 receptor that the coronavirus uses to enter cells. Infection was simulated safely using pseudoviruses that carry the SARS-CoV-2 spike protein along with fluorescent markers, making infected cells easy to detect under a microscope.
Before testing, the team confirmed through immunofluorescence and Western blot analyses that the cells strongly expressed human ACE2, ensuring the model was reliable. They then exposed these cells to different concentrations of bromhexine.
Major Findings Show Strong Antiviral Effects
The key discovery was that bromhexine reduced Omicron pseudovirus infection with an IC50 of just 17.3 micromolar, meaning it cut viral entry by half at relatively low concentration. At 100 micromolar, infections dropped by about 60 percent.
Even more striking, bromhexine also worked against Alpha, Beta and Delta pseudoviruses, reducing infection by about 40 percent at 40 micromolar. This suggests the drug’s antiviral effect is broad and not limited to one strain.
How Bromhexine Blocks the Virus
Using advanced computer modeling and 500 nanosecond molecular dynamics simulations, the researchers showed that bromhexine binds tightly to key sites on the ACE2 receptor. Three amino acids—Phe40, Phe390, and Asn394—played important roles in holding the drug in place through hydrophobic contacts, pi–cation interactions, and hydrogen bonding.
By attaching to ACE2 in this way, bromhexine appears to destabilize the spike–ACE2 interface, blocking the virus from latching onto cells. This mechanism is particularly valuable because it targets the earliest step of infection, reducing the chance for viral replication or mutation.
Why This Matters
Bromhexine is inexpensive, widely available, and already approved for human use as a mucolytic drug. If its antiviral activity can be confirmed in real virus experiments and eventually in clinical trials, it could become an accessible treatment option, especially in countries with limited resources.
Conclusion
The study strongly supports bromhexine as a promising antiviral candidate capable of blocking SARS-CoV-2 entry across multiple variants. Its dual action—interfering with host protease activity and directly disrupting spike-ACE2 binding—gives it unique therapeutic potential. However, more work in animal models and human trials is essential before turning these laboratory findings into clinical solutions. Overall, the research highlights how an affordable repurposed drug may help strengthen global defenses against ongoing and future coronavirus threats.
The study findings were published in the peer reviewed journal: Frontiers in Pharmacology.
Frontiers | Bromhexine inhibits SARS-CoV-2 Omicron and variant pseudovirus infection via ACE2-targeted mechanisms
BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) causes a highly infectious disease characterized by fever, acute respiratory illness, ...
www.frontiersin.org