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56% Of Americans Now Suspect COVID-19 'Vaccines' Caused Mass-Deaths<!-- --> | ZeroHedge

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56% Of Americans Now Suspect COVID-19 'Vaccines' Caused Mass-Deaths
by Tyler Durden
Friday, Mar 13, 2026 - 06:20 PM

Authored by Nicolas Hulscher, MPH,

Public opinion is shifting... and they want action.

A new Rasmussen survey of 1,158 likely U.S. voters - conducted September 7–9, 2025, with a ±3% margin of error - reveals that 56% believe side effects from the COVID-19 shots have likely caused a significant number of unexplained deaths. Nearly one-third (32%) say it’s very likely. Only 35% still dismiss the idea.

This shows that what was once called a “conspiracy theory” has become the mainstream view. The majority of Americans now believe vaccine harms are real and widespread.

Support for HHS Secretary Robert F. Kennedy Jr. reflects this shift. Half of voters (50%) say government health officials deserve criticism for their handling of the pandemic, while 42% even think CDC employees should be fired for their role in misleading the public.

Among those who strongly believe the shots caused deaths, over 70% want CDC firings.

Partisan divides remain—70% of Republicans, 46% of Democrats, and 54% of independents think the vaccines likely caused deaths—but the skepticism crosses party lines and racial groups.

In fact, black (64%) and Hispanic (57%) voters are even more likely than white voters (54%) to suspect deadly vaccine effects.

According to the survey, RFK Jr. is viewed favorably by 45% of voters, with strong support among Republicans and independents, even as Democrats turn sharply against him.

The takeaway: A credible, nationally representative poll now confirms most Americans believe COVID-19 shots have killed many people, and they want accountability from the CDC and government health leaders.
 
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COVID-19 Alters Red Blood Cells Differently by Sex
Medical News Fact checked by:Thailand Medical News Team
Mar 05, 2026

Researchers have uncovered new evidence that COVID-19 does far more than attack the lungs. A new scientific study shows that the virus can significantly alter the metabolism of red blood cells—the cells responsible for transporting oxygen throughout the body—and these changes appear to affect men and women differently.

The research was conducted by scientists from the Vall d’Hebron University Hospital and the Autonomous University of Barcelona in Spain, along with experts from Moldrug AI Systems SL and ProtoQSAR SL located in the Parque Tecnológico de Valencia, Spain. Their findings reveal that COVID-19 can disrupt several crucial metabolic processes inside red blood cells, potentially influencing disease severity and recovery.


Red Blood Cells Under Metabolic Stress
Red blood cells play a critical role in human health by delivering oxygen to tissues and removing carbon dioxide. However, scientists found that SARS-CoV-2 infection causes profound metabolic shifts inside these cells.

By analyzing blood samples from hospitalized COVID-19 patients and comparing them with samples from healthy individuals, researchers discovered widespread disturbances in energy metabolism and antioxidant defenses. Many molecules involved in generating energy and protecting cells from oxidative damage were reduced.

These metabolic disruptions suggest that red blood cells in COVID-19 patients struggle to maintain their normal functions. As a result, oxygen delivery throughout the body may become less efficient, which could partly explain why many patients develop dangerously low oxygen levels.

This Medical News report highlights that the infection does not merely damage tissues directly but also places systemic stress on the body’s metabolic systems.


Clear Differences Between Men and Women
One of the most striking discoveries was that the metabolic changes were more extensive in men than in women. Male patients showed broader alterations in amino acids and energy-related molecules, especially in severe cases of the disease.

For example, levels of several amino acids—including leucine, phenylalanine, lysine, and isoleucine—were significantly reduced in men. These molecules are important for energy balance and cellular repair. Their decline may indicate a stronger metabolic strain in male patients.

In contrast, female patients showed fewer metabolic disruptions overall. However, women displayed changes in specific molecules linked to oxygen release from red blood cells. One key molecule called 2,3-BPG, which helps hemoglobin release oxygen to tissues, was reduced in women with severe COVID-19.

These differences may partly explain why men tend to experience more severe acute illness while women sometimes develop longer-lasting post-COVID symptoms.


Risk Factors Also Influence Blood Metabolism
The researchers also examined how common health conditions such as diabetes, obesity, age, and cardiovascular disease influence these metabolic changes.

They found that these underlying conditions can significantly modify how red blood cells respond to infection. For instance, some metabolic signals detected in healthy individuals with COVID-19 were less visible in patients who also had diabetes or heart disease.

This suggests that pre-existing metabolic stress may interact with the viral infection, altering how the body reacts and possibly affecting disease outcomes.


Potential Pathway Toward New Biomarkers
The study suggests that analyzing the metabolism of red blood cells could become a useful way to monitor COVID-19 severity and identify patients at higher risk of complications.

Because red blood cells circulate throughout the body, their metabolic profile may act as a window into broader systemic stress caused by infection. Scientists believe this approach could eventually help doctors detect metabolic warning signs earlier and improve patient management.


Conclusion
Overall, the research demonstrates that COVID-19 significantly disrupts the metabolism of red blood cells, affecting pathways involved in energy production, oxidative stress protection, and oxygen delivery. These alterations are more pronounced in men, suggesting that biological sex influences how the body metabolically responds to the virus. The findings also show that underlying conditions such as diabetes, obesity, and cardiovascular disease can modify these metabolic patterns. Understanding these differences may help researchers develop better diagnostic markers and therapeutic strategies aimed at protecting red blood cell function and improving outcomes in future viral outbreaks.

The study findings were published in the peer reviewed journal: Biology.
 
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A potential broad coronavirus drug target: Blocking tRNA-modifying enzymes slows viral proteins
by Universitat Pompeu Fabra - Barcelona
edited by Sadie Harley, reviewed by Robert Egan
March 7, 2026

Coronaviruses not only use the machinery of the human cells they infect: they modify them to achieve optimal conditions to produce viral proteins and thus spread more quickly. This is the main conclusion of a study by Pompeu Fabra University published in Nature Communications.

The study identifies enzymes that modify transfer RNAs (tRNAs)—small cellular parts required to build proteins—as key elements for coronavirus infection. These enzymes are activated by the stress response of viral infection and could be a new therapeutic target for developing broad-spectrum antiviral drugs against coronaviruses.

In the last 25 years, the world has witnessed three major outbreaks of coronavirus respiratory diseases that have been passed from animals to humans: SARS-CoV-1 in 2002, MERS in 2012, and SARS-CoV-2 in 2019. While the first two caused epidemics, SARS-CoV-2 triggered a pandemic that caused more than 7 million deaths.

"Coronaviruses are very dangerous because of their ability to generate new variants capable of infecting humans after circulating in animal reservoirs," explains Juana Díez, director of the Molecular Virology Research Group at Pompeu Fabra University, who led the research.

"At present, we do not have any broad-spectrum antiviral drugs that are effective against coronaviruses. So when a new coronavirus emerges, a scenario considered highly likely among the scientific community, we will be in the same position as at the end of 2019, when we did not have the drugs to control the spread of the virus."

Like any other virus, coronaviruses use the machinery of the cells they infect to make viral proteins and spread. In this process, tRNAs—very small cellular parts that add amino acids to the new protein based on the information they read in the RNA—are key.

"Interestingly, coronaviruses need tRNAs that are in low concentrations in cells. For this reason, we asked ourselves how a virus can spread so quickly within a cell where the tRNAs it needs to make its viral proteins are not abundant," outlines Elena Muscolino, first author of the study.
Taking advantage of change

The study published in Nature Communications shows that infection causes stress that chemically alters tRNAs and changes the functioning of the cellular machinery. Thus, the cell is no longer optimized to produce its own proteins and acquires the ideal conditions to respond to stress.

Coronaviruses have taken advantage of this situation, since "in order to manufacture stress response proteins, the same tRNAs that coronaviruses need to manufacture their viral proteins are needed," explains Mireia Puig, also an author of the work.

This readjustment, driven by cellular enzymes that modify tRNAs, allows coronaviruses to speed up the production of their proteins without the need to generate new machinery, simply by altering the existing one.

"Since changes in tRNAs are modifications of the machinery that the cell already has and not the generation of new 'cell parts," viral protein production occurs rapidly and coronaviruses can spread very quickly," Muscolino points out.

The modification of tRNAs has been observed both in SARS-CoV-2, associated with serious infections, and in HCoV-OC43, which usually causes very mild cold-like signs and symptoms. Therefore, it could be a common strategy among different coronaviruses. In addition, when the activity of these modifying enzymes is blocked, viral protein production decreases significantly.

"The tRNA-modifying enzyme is a promising candidate for developing broad-spectrum antiviral drugs capable of curbing the spread of coronaviruses," Díez states. And she adds, "A drug of this type would allow us to contain the infections caused by new coronaviruses from their initial phases and prevent their rapid expansion, and therefore, new pandemics."

This study, led by Pompeu Fabra University, was carried out in collaboration with the research groups led by Arvind H. Patel and Alfredo Castelló (University of Glasgow), Rafael Sanjuán (Institute for Integrative Systems Biology, Valencia), and Miguel Chillón (Autonomous University of Barcelona).

Publication details
Elena Muscolino et al, Coronaviruses reprogram the tRNA epitranscriptome to favor viral protein expression, Nature Communications (2026). DOI: 10.1038/s41467-026-69700-w
Journal information: Nature Communications
Provided by Universitat Pompeu Fabra - Barcelona
 
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A Bad Case of COVID or Flu May Raise Lung Cancer Risk Years Later
By University of Virginia Health System
March 11, 2026

Severe COVID or flu may quietly raise lung cancer risk—but vaccines appear to stop the damage before it starts.

New research from UVA Health’s Beirne B. Carter Center for Immunology Research and the UVA Comprehensive Cancer Center suggests that severe cases of COVID-19 and influenza may create conditions in the lungs that make cancer more likely to develop later. The study also found that vaccination appears to prevent these harmful effects.

Researchers at the UVA School of Medicine, led by Jie Sun, PhD, discovered that serious viral infections can alter immune cells in the lungs in ways that promote tumor growth months or even years afterward. Based on these findings, the team recommends that doctors closely monitor patients who have recovered from severe COVID, flu, or pneumonia so lung cancer can be detected early, when treatment is most effective.

“A bad case of COVID or flu can leave the lungs in a long-lasting ‘inflamed’ state that makes it easier for cancer to take hold later,” said Sun, co-director of UVA’s Carter Center and a member of UVA’s Division of Infectious Diseases and International Health. “The encouraging news is that vaccination largely prevents those harmful changes for cancer growth in the lung.”


How Severe Viral Infections Can Set the Stage for Lung Cancer

Respiratory illnesses such as influenza and COVID are among the leading causes of lung injury. However, scientists have not fully understood how these injuries might affect cancer risk over the long term. To investigate, Sun and his colleagues studied the effects of severe infections in both laboratory mice and human patients.

The findings were striking. Mice that experienced severe lung infections were more likely to develop lung cancer later and were also more likely to die from the disease. When researchers examined patient data, they observed a similar pattern. Individuals who had previously been hospitalized with COVID-19 showed a higher rate of lung cancer diagnoses.

Overall, hospitalization for COVID-19 was associated with a 1.24-fold increase in lung cancer risk. This increase appeared regardless of whether patients smoked or had other health conditions, which doctors call “comorbidities.”

“These findings have important immediate implications for how we monitor patients after severe respiratory viral infection,” said Jeffrey Sturek, MD, PhD, a UVA physician-scientist who collaborated on the study. “We’ve known for a long time that things like smoking increase the risk for lung cancer. The results from this study suggest that we may need to think about severe respiratory viral infection similarly. For example, in some patients who are at high risk for lung cancer based on smoking history, we recommend close monitoring with routine screening CT scans of the lungs to catch cancer early. In future studies, we may want to consider a similar approach after severe respiratory viral infection.”


Immune Changes That Help Tumors Grow

Experiments in mice helped researchers understand why this increased risk occurs. Severe viral infections caused major changes in immune cells known as neutrophils and macrophages, which normally protect lung tissue.

After infection, some neutrophils behaved abnormally and contributed to a persistent inflammatory environment that favors tumor growth. Scientists also observed significant alterations in epithelial cells, the cells that line the lungs and the air sacs responsible for breathing.


Vaccination May Prevent Cancer-Promoting Lung Changes

The researchers found encouraging evidence that vaccination can block these harmful biological changes. Vaccines train the immune system to respond quickly to infections, which helps reduce how severe the illness becomes.

The increased lung cancer risk was seen in patients who experienced severe COVID-19, but not in those who had mild cases. In fact, people with mild infections showed a small decrease in risk.

Despite this protective effect, the researchers caution that millions of people who survived severe COVID-19 or other serious respiratory infections could face an elevated risk of lung cancer in the future.

“With tens of millions of people globally experiencing long-term pulmonary [COVID-19] sequelae, these findings carry significant implications for clinical care,” the scientists wrote in their paper. “Individuals recovering from severe viral pneumonia, particularly those with smoking history, may benefit from enhanced lung cancer surveillance, and preventing severe infection through vaccination may confer indirect cancer protection benefits.”


Implications for Early Detection and Future Treatments

Sun and his team hope their work will help doctors identify patients who may face a higher risk of lung cancer after severe viral infections. Earlier identification could allow patients to receive screening and treatment sooner.

The researchers also believe their findings could guide the development of new therapies aimed at counteracting the biological changes caused by severe lung infections.

“Our goal is to help doctors identify who may be at higher risk of lung cancer after a severe infection, and develop targeted ways to prevent and treat lung cancer after prior pneumonia,” Sun said. “We also believe that vaccines don’t just prevent acute hospitalization after contracting the virus. They may also reduce the long-term fallout of severe infection, including the kind of immune scarring that can increase cancer risk.”

Reference: 11 March 2026, Cell.

The findings were published in the scientific journal Cell.

The research team included Wei Qian, Xiaoqin Wei, Andrew J. Barros, Xiangyu Ye, Haibo Zhang, Qing Yu, Samuel P. Young, Eric V Yeatts, Yury Park, Chaofan Li, Sijie Hao, Gislane Almeida-Santos, Jinyi Tang, Harish Narasimhan, Nicole A Kirk, Valeria Molinary, Ying Li, Li Li, Bimal N. Desai, Peter Chen, Kwon-Sik Park, Anny Xiaobo, Jeffrey M. Sturek, Wei Chen, In Su Cheon, and Sun.

Understanding and treating complex diseases is a major focus of UVA’s Paul and Diane Manning Institute of Biotechnology. The institute works to accelerate discoveries like Sun’s research and translate them more quickly into new medical treatments that can save lives.

UVA’s Beirne B. Carter Center for Immunology Research (CIC) was established through the generosity of Beirne B. Carter, and the Beirne Carter Foundation continues to support its work. CIC scientists study infections, cancer, cardiovascular disease, chronic lung conditions, the microbiome, and autoimmune disorders to advance new therapies and cures.

The UVA Comprehensive Cancer Center is one of only 57 cancer centers nationwide to receive the National Cancer Center’s “comprehensive” designation, recognizing excellence in patient care and innovative cancer research.

Funding for the research came from the National Institutes of Health, grants AI147394, AG069264, AI112844, HL170961, AI176171, AG090337, R01HL179312, F31HL170746, T32AI007496, T32CA009109, R01AI155808 and R01HL162783; a UVA Comprehensive Cancer Center Collaborative Grant, U01CA224293; a UVA Pinn Scholar Award; a UVA Shannon Fellowship; a UVA Comprehensive Cancer Center Lung TRT Pilot Grant; an American Lung Association Catalyst Grant, T32GM139787-01; and a UVA Parsons-Weber-Parsons Fellowship.
 
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Beyond mRNA: Scientists Turn DNA Origami Into a Powerful New Vaccine Platform
By Benjamin Boettner, Wyss Institute for Biologically Inspired Engineering at Harvard
March 11, 20261

Scientists have developed a new DNA origami–based vaccine platform called DoriVac that could rival mRNA vaccines while being easier to manufacture and store. Early studies show it can trigger strong immune responses against viruses like SARS-CoV-2, HIV, and Ebola.

The COVID-19 pandemic pushed messenger RNA (mRNA) vaccines into the spotlight of global health. After completing clinical trials, the first COVID-19 mRNA vaccine was administered on 8 December 2020. Modeling studies later estimated that these vaccines prevented at least 14.4 million deaths from COVID-19 during their first year of use.

Their strong performance against the virus also sparked efforts to apply mRNA technology to other diseases. Clinical trials are now underway for vaccines targeting influenza virus, Respiratory Syncytial Virus (RSV), HIV, Zika, Epstein-Barr virus, and tuberculosis bacteria. At the same time, research conducted during the pandemic has revealed several limitations of mRNA vaccines that point to the need for alternative strategies.

Limitations of Current mRNA Vaccine Technology

The immune protection generated by COVID-19 mRNA vaccines can differ widely among individuals, and the protection tends to decline over time. The challenge becomes even greater because the SARS-CoV-2 virus continually evolves, producing new variants that can partially evade immune defenses. As a result, COVID-19 vaccines often need periodic updates.

Additional drawbacks exist as well. Manufacturing these vaccines can be complex and expensive, and scientists have limited control over the number of mRNA molecules packaged inside the lipid nanoparticles used for delivery. These vaccines also require cold storage and may sometimes cause unintended off-target effects. Addressing these issues could open the door to improved prevention, faster response, and better preparedness for a wide range of infectious diseases.

A DNA Origami Vaccine Platform Called DoriVac

A multidisciplinary team from the Wyss Institute at Harvard University, Dana-Farber Cancer Institute (DFCI), and collaborating institutions has explored a different approach. They used a recently developed DNA origami nanotechnology platform called DoriVac that functions as both a vaccine and an adjuvant.

In their experiments, DoriVac vaccines targeted a peptide region (HR2) that is conserved within the spike proteins of several viruses, including SARS-CoV-2, HIV, and Ebola. In mice, the SARS-CoV-2 HR2 version of the vaccine triggered strong immune activity. This included antigen-specific antibody responses (humoral immunity) and T cell responses (cellular immunity).

The researchers also evaluated the vaccine using an advanced preclinical system that models the human immune system. Using the Wyss Institute’s microfluidic human Organ Chip technology, they created an in vitro model of the human lymph node. Within this system, the SARS-CoV-2 HR2 vaccine also produced strong antigen-specific immune responses in human cells.

In a direct comparison with SARS-CoV-2 mRNA vaccines delivered in lipid nanoparticles, a DoriVac vaccine carrying the same spike protein variant produced a similarly strong activation of the human immune system. However, the DNA origami vaccine proved to be more stable and easier to store and manufacture. The findings were published in Nature Biomedical Engineering.

“With the DoriVac platform, we have developed an extremely flexible chassis with a number of critical advantages, including an unprecedented control over vaccine composition, and the ability to program immune recognition in targeted immune cells on a molecular level to achieve better responses,” said co-corresponding author and Wyss Institute Core Faculty member William Shih, Ph.D., whose group pioneered the new vaccine concept. “Our study demonstrates DoriVac’s versatility and potential by taking a close look at the immune changes that are required to fight infectious viruses.” Shih is also Professor at the Harvard Medical School and DFCI.

Bringing Viral Antigens Into the Fold

In 2024, Shih’s group at the Wyss Institute and Dana-Farber introduced DoriVac as a broadly applicable vaccine platform based on DNA nanotechnology. Yang (Claire) Zeng, M.D., Ph.D., who led the project with collaborators, showed that the technology could present immune-boosting adjuvant molecules to cells with nanometer-level precision.

In earlier work involving tumor-bearing mice, DoriVac vaccines produced stronger immune responses than versions that lacked the DNA origami structure. The vaccine design relies on small self-assembling square nanostructures made of DNA. One side of the structure displays adjuvant molecules arranged at carefully optimized nanometer spacing. The opposite side presents selected antigens such as peptides or proteins derived from tumors or pathogens.

“While we were developing the platform for cancer applications, the COVID-19 pandemic was still moving with full force. So, the question quickly arose whether DoriVac’s superior adjuvant activity could also be leveraged in infectious disease settings,” said Zeng as a first and co-corresponding author on the new study, and now cofounder and CEO/CTO of DoriNano, leading the translation of this technology into clinical applications.

To explore that possibility, Zeng and co-first author Olivia Young, Ph.D., a former graduate student in Shih’s group, collaborated with Donald Ingber’s team at the Wyss Institute. Ingber’s group focuses on developing antiviral therapies using AI-driven and multiomics approaches alongside microfluidic human Organ Chip technology. Working with co-first author Longlong Si, Ph.D., a former postdoctoral researcher in Ingber’s lab, the researchers created DoriVac vaccines targeting SARS-CoV-2, HIV, and Ebola. These vaccines display HR2 peptides, which serve as conserved antigens within the spike proteins of several viruses.

“Our analysis of the immune responses provoked by these first DoriVac vaccines in mice led to several encouraging observations, including significantly greater and broader activation of humoral and cellular immunity across a range of relevant immune cell types than what the origami-free antigens and adjuvants could produce,” said Zeng. “We found that the numbers of antibody-producing B cells, activated antigen-presenting dendritic cells (DCs), and antigen-specific memory and cytotoxic T cell types that are vital for long-term protection were all increased, especially in the case of the SARS-CoV-2 HR2,” explained Zeng.

Moving From Mouse Models Toward Human Systems

Immune responses in mice can differ significantly from those in humans. Because of this, many treatments that appear promising in mouse studies fail during human clinical trials. To bridge that gap, the researchers tested their vaccines in a more human-like system.

They used a human lymph node-on-a-chip (human LN Chip), an engineered microfluidic system that mimics aspects of the human immune system. This platform allows scientists to predict immune responses in humans more efficiently during early-stage testing.

Developed by co-first author Min Wen Ku and co-corresponding author Girija Goyal, Ph.D., Director of Bioinspired Therapeutics at the Wyss Institute, the system showed that the SARS-CoV-2-HR2 DoriVac vaccine activated human DCs and significantly increased the production of inflammatory cytokine molecules compared with origami-free vaccine components. The number of CD4+ and CD8+ T cells with multiple protective functions also rose in the human LN Chips, further supporting the potential of DoriVac vaccines for human use.

“The predictive capabilities of human LN Chips gave us an ideal testing ground for DoriVac vaccines and the induced, antigen-specific immune cell profiles and activities very likely reflect those that would occur in human recipients of the vaccines. This convergence of technologies enabled us to dramatically raise the chances of success for a new class of vaccines and create a new testbed for future vaccine developments,” said co-corresponding author Ingber, M.D., Ph.D. who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Boston Children’s Hospital, and the Hansjörg Wyss Professor of Biologically Inspired Engineering at Harvard John A. Paulson School of Engineering and Applied Sciences.

Comparing DNA Origami Vaccines With mRNA Vaccines

The researchers also studied a DoriVac vaccine displaying the full SARS-CoV-2 spike protein. Led by Zeng and co-author Qiancheng Xiong, the team compared it directly with Moderna and Pfizer/BioNTech mRNA lipid nanoparticle (LNP) vaccines that encode the same spike protein.

In mice that received a standard booster protocol, the DNA origami vaccine generated antiviral T cell responses and antibody-producing B cell responses that were comparable to those produced by the mRNA vaccines.

“This underscored DoriVac’s potential as a DNA nanotechnology-enabled, self-adjuvanted vaccine platform. But DoriVac vaccines have a number of other advantages: they don’t have the same cold-chain requirements as mRNA-LNP vaccines do and thus could be distributed much more effectively, especially in under-resourced regions; and they could overcome some of the enormous manufacturing complexities of LNP-formulated vaccines, to name two major ones,” said Shih. Recent studies at DoriNano have also demonstrated that DoriVac exhibits a promising safety profile.

Reference: “DNA origami vaccine nanoparticles improve humoral and cellular immune responses to infectious diseases” 11 March 2026, Nature Biomedical Engineering.

Other authors on the study are Sylvie Bernier, Hawa Dembele, Giorgia Isinelli, Tal Gilboa, Zoe Swank, Su Hyun Seok, Anjali Rajwar, Amanda Jiang, Yunhao Zhai, LaTonya Williams, Caleb Hellman, Chris Wintersinger, Amanda Graveline, Andyna Vernet, Melinda Sanchez, Sarai Bardales, Georgia Tomaras, Ju Hee Ryu, and Ick Chan Kwon. The study was supported by funding from the Director’s Fund and Validation Project program of the Wyss Institute; Claudia Adams Barr Program at DFCI; National Institutes of Health (U54 grant CA244726-01); US-Japan CRDF global fund (grant R-202105-67765); National Research Foundation of Korea (grants MSIT, RS-2024-00463774, RS-2023-00275456); Intramural Research Program of the Korea Institute of Science and Technology (KIST); and Bill and Melinda Gates Foundation (INV-002274).
 
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COVID-19 Infection Linked to Immune Changes That May Influence Cancer
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 12, 2026

Researchers are increasingly examining how COVID-19 affects the body beyond the initial infection. A new scientific review suggests that while the SARS-CoV-2 virus does not directly cause cancer, it can disturb the immune system in ways that may temporarily create conditions that allow existing tumors to grow or spread more easily.

How COVID-19 Disrupts the Immune System
Scientists from the Institute of Microbiology and Virology at Riga Stradins University in Riga, Latvia examined how COVID-19 infection affects immune responses and how these changes may interact with cancer-related biological pathways.

The researchers found that SARS-CoV-2 can trigger a powerful immune reaction in some people. Normally, when viruses enter the body, immune cells release protective molecules called interferons that help stop viral replication. However, in severe COVID-19 cases, this early response is often delayed or weakened.

When that happens, another powerful inflammatory pathway known as NF-kB signaling becomes highly active. This leads to the release of large amounts of inflammatory molecules such as IL-6, TNF-alpha and IL-1 beta. The excessive immune response—often described as a cytokine storm—can damage tissues and disturb normal immune regulation.

From Acute Infection to Long-Term Immune Imbalance
According to the researchers, the immune disruption caused by COVID-19 does not always disappear immediately after recovery. In some individuals, low-level inflammation can persist for months.

This lingering immune imbalance has been observed in people with long COVID. Studies have shown elevated inflammatory markers and altered immune cell populations long after the virus has cleared. For example, some patients experience reduced numbers of naïve immune cells and increased levels of exhausted T-cells—immune cells that have lost some of their ability to fight infections or abnormal cells.

This Medical News report highlights that such immune exhaustion may reduce the body’s ability to detect and eliminate abnormal cells, including potential cancer cells.

Viral Proteins That Activate Cancer-Related Pathways
The study also explains that certain proteins produced by SARS-CoV-2 can interact with cellular signaling networks inside human cells.

For instance, the spike protein can activate immune receptors that trigger inflammation through NF-kB and MAPK pathways. These same pathways are known to play roles in cell growth, inflammation and survival—processes that are also involved in cancer development.

Another viral component, called the membrane protein, has been shown in laboratory studies to stimulate signaling pathways that influence cellular migration and tissue remodeling. These changes do not directly create cancer but may strengthen biological pathways that tumors already use to grow.

Effects on Tumor Environments
The researchers also reviewed evidence showing that COVID-19-related inflammation may alter the tumor microenvironment—the complex network of immune cells, blood vessels and signaling molecules surrounding tumors.

Persistent inflammation may encourage the production of molecules that help tumors avoid immune detection. It may also stimulate processes such as angiogenesis, where tumors develop new blood vessels to support growth.

In animal models, lung inflammation caused by SARS-CoV-2 infection has even been shown to awaken dormant cancer cells and trigger metastatic growth, though this effect appears to depend heavily on individual immune conditions.

Conclusion
Overall, the researchers stress that SARS-CoV-2 is not a cancer-causing virus. Instead, it should be viewed as a temporary immune stressor that can disrupt inflammatory and immune pathways already involved in tumor biology. Severe infections and prolonged inflammation may create conditions that temporarily weaken immune surveillance or enhance tumor-supportive signals in vulnerable individuals. Continued long-term studies are still needed to understand how post-COVID immune changes may influence cancer outcomes over time.

The study findings were published in the peer reviewed journal: Vaccines.
 
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COVID-19 Infections Rising in Virginia and Arizona Sparks New Concerns Across United States
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 12, 2026


Medical News: CDC Data Signals Localized Growth in Infections
New modeling data released by the Centers for Disease Control and Prevention indicates that COVID-19 infections are beginning to rise again in select regions of the United States, particularly in the states of Virginia and Arizona. Although the national outlook currently shows declining or stable trends in most states, public health analysts say the emerging increases highlight how localized outbreaks can still occur even when overall national indicators appear relatively stable.

As of March 3, 2026, CDC modeling estimates suggest that infections are growing or likely growing in two states. In contrast, COVID-19 cases are declining or likely declining in 35 states, while 10 states are showing little to no significant change. The agency continues to rely on a combination of clinical reporting, predictive modeling, and wastewater surveillance to track transmission trends across the country.


Wastewater Surveillance and Modeling Reveal Early Warning Signs
One of the key surveillance tools currently being used by the CDC involves wastewater monitoring systems. These systems analyze viral genetic material present in sewage, providing an early indicator of community spread even before large numbers of clinical cases are reported. Public health experts say this method has become an essential component of pandemic monitoring since many infections are now mild and may go unreported.

According to the CDC’s forecasting and Rt estimation models, the reproductive rate of the virus in certain communities within Virginia and Arizona has edged above the threshold that indicates sustained transmission. When this rate rises above 1, each infected individual transmits the virus to more than one person on average, allowing outbreaks to gradually expand.


Hospitals Report Gradual Uptick in Some Regions
While official CDC modeling highlights Virginia and Arizona, clinicians in Maryland have also begun reporting a slow but noticeable increase in COVID-19 cases among patients seeking treatment. Some hospitals have observed slightly higher emergency visits associated with respiratory symptoms over the past several weeks.

Doctors emphasize that the increases remain modest compared to earlier pandemic waves, but they are closely monitoring the situation as seasonal respiratory viruses and emerging variants continue to circulate.


Emerging Variants Circulating in The United States
Virological surveillance also shows that several SARS-CoV-2 lineages are currently circulating in the United States. Among the most frequently detected strains are XFG.1.1, followed by PQ.2.8.1 and PQ.17. Researchers are continuing to monitor these variants to determine whether they possess advantages in transmissibility or immune escape.

Within this Medical News report, experts stress that while these variants do not currently appear to cause more severe disease, their ability to spread efficiently could still influence regional infection trends.


Public Health Experts Urge Continued Vigilance
Health officials stress that although most U.S. states are experiencing stable or declining COVID-19 activity, the situation demonstrates that the virus remains unpredictable and capable of resurging in localized pockets. Continued surveillance, testing in healthcare settings, and genomic monitoring remain critical tools for detecting early warning signs of potential outbreaks.

Researchers note that even modest increases in transmission can rapidly evolve if surveillance and response systems are weakened. Maintaining public health awareness, encouraging vaccination updates for high-risk populations, and monitoring hospital trends remain essential strategies to prevent localized surges from expanding into broader regional waves. The current data underscores that COVID-19 has transitioned into a persistent endemic threat that still requires active monitoring, rapid reporting systems, and coordinated healthcare responses across states.


Reference:
www.cdc.gov

Current Epidemic Trends (Based on Rt) for States

CFA’s Rt page estimates COVID-19, influenza, and RSV epidemic trends for U.S. states.
www.cdc.gov www.cdc.gov
 
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CDC Buried COVID Vaccine Death Data in Lancet Study, Internal Documents Reveal

CDC researchers altered their own study on COVID-19 vaccine adverse events to downplay deaths linked to the shots, according to documents obtained by Children’s Health Defense. CHD sued the CDC in 2023 to obtain the documents after the agency failed to respond to CHD’s Freedom of Information Act...
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CDC Buried COVID Vaccine Death Data in Lancet Study, Internal Documents Reveal
CDC researchers altered their own study on COVID-19 vaccine adverse events to downplay deaths linked to the shots, according to documents obtained by Children’s Health Defense. CHD sued the CDC in 2023 to obtain the documents after the agency failed to respond to CHD’s Freedom of Information Act request.
by Suzanne Burdick, Ph.D.
March 19, 2026

Researchers with the Centers for Disease Control and Prevention (CDC) altered their own study on COVID-19 vaccine adverse events to downplay deaths linked to the shots, according to documents obtained by Children’s Health Defense (CHD).

CHD sued the CDC in 2023 to obtain the documents after the agency failed to respond to CHD’s Freedom of Information Act (FOIA) request.

The 100-page document tranche included an earlier draft of the CDC study that differed significantly from the version the authors published in June 2022 in The Lancet Infectious Diseases.

Karl Jablonowski, Ph.D., CHD senior research scientist, who analyzed the FOIA documents, said the CDC “severely edited” the study “to promote safety and to de-emphasize death.”

The first four words of the draft’s title were “Reactogenicity and Adverse Events.” However, the published version’s title began with “Safety of mRNA vaccines.”

Reactogenicity refers to the side effects or adverse events someone experiences after taking a vaccine or medication.

The study authors, members of the CDC’s COVID-19 Response Team, analyzed reports of adverse events following mRNA COVID-19 vaccination during the first 6 months of the vaccine rollout in the U.S.

The researchers pulled the reports from two federal vaccine safety monitoring systems — the Vaccine Adverse Event Reporting System (VAERS) and V-safe.

Although there were 4,496 deaths reported to VAERS during that time frame, the study authors stripped details about the deaths from the article’s abstract.

The lead study author, Dr. Hannah Rosenblum, wrote in a comment on the draft, “Note all death results/interpretation has been removed from abstract.”

That’s a big deal, Jablonowski said — because the abstract, which appears at the top of a study and summarizes it, is typically read much more than the full body of an article.

The published version also omitted a figure that revealed key statistics about deaths reported following COVID-19 vaccination to VAERS. The figure depicted the percentage breakdown for the top 10 leading causes of death — including diseases of the heart, COVID-19 disease and “unknown/unclear” — as listed on death certificates or autopsy results.

The draft also originally included a table showing similar information, Jablonowski said. “But when the authors published the study, they buried the table in the study’s supplemental materials, where it was sure to be read by very few.”

Although the CDC and the U.S. Food and Drug Administration (FDA) contributed to the study, the article included the disclaimer that its findings and conclusions “are those of the authors and do not necessarily represent the official position of the CDC or the FDA.”

Study author under investigation for allegedly destroying records on COVID vaccine adverse events

The FOIA results come at a time of renewed scrutiny over the CDC’s handling of COVID-19 vaccines and adverse events, including death, associated with the shots.

The CDC’s vaccine advisory panel had planned to discuss COVID-19 vaccine injuries at its meeting this week. However, a federal judge on March 16 blocked the meeting.

Jablonowski said it was unethical that the CDC study authors altered their manuscript to emphasize safety and downplay death. He said:

“When the study was published, America was weighing whether or not to get a booster, or perhaps a second booster dose. They had to weigh what the Trusted News Initiative was telling us about the shots being ‘safe and effective.’

“Is it really 95% effective if we still get sick and need a booster every few months? Could the sudden surge of people dying suddenly have anything to do with the vaccine’s safety?”

A CDC study that “honestly and clearly” conveyed the risks of adverse events and death associated with the shot would have helped the public make a decision, Jablonowski said.

One in 10 U.S. adults who received a COVID-19 vaccine suffered “major” side effects, and over a third (36%) experienced “minor” side effects, according to a national survey conducted in November 2025.

Based on a U.S. adult population of 258 million in 2020, the results mean that about 17 million adults who got a COVID-19 vaccine experienced major health effects, and roughly 63 million had minor side effects, said Rasmussen Reports, which conducted the survey.

Dr. Tom Shimabukuro, former director of the CDC Immunization Safety Office and one of the study’s authors, has been referred to the U.S. Department of Justice, the FBI and the Office of Inspector General for allegedly deleting or destroying agency records and communications related to COVID-19 vaccine adverse events.

In an April 2025 letter, Sen. Ron Johnson (R-Wis.) called on the agencies to investigate Shimabukuro.

Study authors claim COVID vaccine death pattern ‘similar’ to other vaccines

The CDC study downplayed deaths potentially caused by the COVID-19 vaccines in other ways, too, Jablonowski said.

For instance, the study states, “The concentrated reporting of deaths on the first few days after vaccination follows patterns similar to those observed for other adult vaccinations.”

The study authors didn’t provide information on what a typical pattern of death following other vaccines looks like, Jablonowski said. “So I downloaded VAERS data and plotted the curves myself.”

adult-deaths-covid-vaccination-chart.jpg


The curves showed that death reports decreased over time following both COVID-19 vaccines and other vaccines. However, the number of death reports following COVID-19 vaccinations was higher than those reported after other vaccines.

The CDC study authors also tried to dismiss the high concentration of deaths reported following COVID-19 vaccination by insinuating that the VAERS reports were biased. They wrote:

“This pattern might represent reporting bias because the likelihood to report a serious adverse event might increase when it occurs in close temporal proximity to vaccination.”

At least one commenter on the draft pushed back on dismissing the patterns of VAERS death reports as being a result of reporting bias. A person with the initials B.R. commented in the draft that a VAERS death report filed soon after a person received a COVID-19 vaccine “may also reflect a true event.”

Jablonowski suggested the individual was likely Dr. Robert Ball, the deputy director of the FDA’s Office of Surveillance and Epidemiology at its Center for Drug Evaluation and Research.

It’s unclear if Ball initially served as a draft author, as the CDC redacted some of the draft authors’ names in its FOIA response. Ball was not listed as an author of the final publication.

Ball did not immediately respond when asked if he had been involved in the study.

Study authors mum on why they changed the study

When the study was published, all its authors were members of the CDC’s COVID-19 Response Team.

It’s unclear how many of them still work at the CDC.

However, it is clear that the CDC does not want the study authors to publicly comment on why they altered their manuscript before publishing it.

When The Defender asked the study’s corresponding author, Julianne Gee, why she and her co-authors removed all death results from the abstract, a CDC public affairs specialist referred The Defender to the U.S. Department of Health and Human Services (HHS).

HHS did not respond by the deadline.
 
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Researchers Find a Surprising Long COVID Clue in Major Vitamin D Trial
By Mass General Brigham
March 12, 2026

Vitamin D didn’t blunt COVID’s initial impact—but it may hold a surprising clue in the fight against long COVID.

A large randomized study led by researchers at Mass General Brigham found that taking high doses of vitamin D3 did not lessen the severity of COVID-19 infections. However, the results suggest the supplement could play a role in long COVID outcomes. The findings were published in The Journal of Nutrition.

“There’s been tremendous interest in whether vitamin D supplements can be of benefit in COVID, and this is one of the largest and most rigorous randomized trials on the subject,” said senior author JoAnn Manson, MD, DrPH, of the Mass General Brigham Department of Medicine. “While we didn’t find that high-dose vitamin D reduced COVID severity or hospitalizations, we observed a promising signal for long COVID that merits additional research.”


The VIVID Trial Design and Participants

Vitamin D has long been studied for its potential effects on immune health, though research related to COVID-19 has produced inconsistent results. To better understand whether supplementation could help, scientists launched the Vitamin D for COVID-19 (VIVID) Trial. The study carefully evaluated the impact of high-dose vitamin D3 supplements among people recently diagnosed with COVID-19, as well as members of their households.

The trial included participants from both the United States and Mongolia. In total, 1,747 adults who had recently tested positive for COVID-19 and 277 household contacts were randomly assigned to receive either vitamin D3 or a placebo for four weeks. The supplementation regimen consisted of vitamin D3 (9,600 IU/day for two days followed by 3,200 IU/day).

The U.S. portion of the trial ran from December 2020 through September 2022. The Mongolia study took place between September 2021 and April 2022. On average, participants began taking vitamin D or a placebo about three days after receiving a positive COVID-19 test result.


Ensuring Balanced Study Groups

Lead authors Davaasambuu Ganmaa and Kaitlyn Cook worked alongside Manson and the research team to ensure the study groups were comparable. The researchers used stratified randomization and statistical weighting to balance factors that could influence COVID-19 outcomes (including age, sex, body mass index, race/ethnicity and COVID-19 vaccination status).


No Change in COVID-19 Severity or Transmission

After four weeks, the study found no difference between the vitamin D and placebo groups in terms of healthcare use or death. Healthcare utilization included hospitalizations, clinic visits either in person or virtual, and emergency department visits. Researchers also saw no meaningful difference in symptom severity.

In addition, vitamin D supplementation did not lower the likelihood that household contacts would become infected with COVID-19.


Possible Signal for Reduced Long COVID Symptoms

Although vitamin D did not improve short-term COVID-19 outcomes, researchers noticed a possible connection with long COVID when they looked at participants who consistently followed the supplement regimen. These individuals appeared somewhat less likely to report lingering symptoms eight weeks after infection.

Among those taking vitamin D, 21% reported at least one ongoing symptom compared with 25% in the placebo group. The difference was considered borderline statistically significant.

“Long COVID, which can include symptoms of fatigue, shortness of breath, brain fog, other cognitive challenges and more, continues to significantly impact people’s lives,” said Manson. “We hope to conduct further research in larger populations on whether long-term vitamin D supplementation reduces the risks and severity of long COVID.”

Reference: “A Randomized Trial of Vitamin D Supplementation and COVID-19 Clinical Outcomes and Long COVID: The VIVID Trial” 12 March 2026, Journal of Nutrition.
DOI: 10.1016/j.tjnut.2026.101398

Authorship: In addition to Manson and Ganmaa, Mass General Brigham authors include Allison Clar, Michael Rueschman, Aditi Hazra, Howard D. Sesso, Valerie E. Stone, Patricia Copeland and Georgina Friedenberg. Additional authors include Cook, Polyna Khudyakov, Dorjbal Enkhjargal, Tsolmon Bilegtsaikhan, Kenneth H. Mayer, Raji Balasubramanian, Douglas C. Smith, Quanhong Lei, Todd Lee, Emily G. McDonald, Tserenkhuu Enkhtsetseg, Erdenebaatar Sumiya, Yansanjav Narankhuu, Myagmarsuren Erdenetuya, Dalkh Tserendagva, Rikard Landberg, Niclas Roxhed, and Susanne Rautiainen.

Disclosures: Roxhed is a founder and shareholder of Capitainer AB, a company commercializing the blood collection devices used in this study. All other authors declare no conflicts of interest.

Funding: The study received anonymous foundation support and philanthropic support from Jon Sabes of Minneapolis, Minn. The authors also acknowledge support from the Tishcon Corporation, which donated the vitamin D and placebo study capsules; Takeda; and Capitainer cards. The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or nonprofit sectors.
 
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Brazil is Facing A COVID-19 Resurgence with Almost 20,000 New Cases in Late February According to WHO Data
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 14, 2026

In a stark reminder that SARS-CoV-2 has not vanished, Brazil is witnessing a noticeable rise in COVID-19 cases in 2026, sparking fresh concerns among health officials and the public. Once the hardest-hit nation during the pandemic's peak years, the country now reports a relative surge that stands out in global data, even as absolute numbers remain far below historical highs. This Medical News report highlights the key indicators driving the renewed attention.


Sharp Jump in Reported Cases
The World Health Organization's latest comprehensive surveillance, covering the 28 days to February 22, 2026, shows Brazil leading with 19.9k confirmed cases—roughly 19,900—out of a global total of about 48.7k.

COVID-19 cases | WHO COVID-19 dashboard

The latest data for coronavirus (COVID-19) cases from the WHO COVID-19 dashboard.
data.who.int data.who.int

This figure represents a significant portion of worldwide reports and indicates an increase from the prior 28-day window, where Brazil's tally was lower (prior period around 11k cases in some comparative snapshots, contributing to a notable uptick of over 70% in some analyses). The data underscores Brazil's outsized role in the modest global fluctuations observed.


Underlying Trends and Surveillance Insights
Brazilian health authorities, through Fiocruz and the Ministry of Health, have tracked rises in severe acute respiratory infections (SRAG) linked to COVID-19 in states such as São Paulo, Rio de Janeiro, Goiás, and others.

Weekly epidemiological bulletins (e.g., SE 08 and SE 09 for late February/early March 2026) describe "leve aumento" (slight increases) in notifications, with positivity rates low but showing upward tendencies in select regions. Latest data ending early March also shows a rise in COVID-19 Infections.


https://www.gov.br/saude/pt-br/assu...s-tecnicas/informes/informe-se-09-de-2026.pdf

https://oglobo.globo.com/saude/noti...a-em-tres-estados-do-brasil-saiba-quais.ghtml


Broader Context and Overall Risk
While the February-March period shows localized upticks, reduced routine testing across the country means figures likely undercount true circulation, relying more on sentinel and wastewater data.

Local doctors and hospitals are warning that he actual true amounts might be much higher compared to the officially reported figures. Due to lack of genomic sequencing and relevant data, what variants are driving the new surge of COVID-19 in Brazil has not been identified. It is also premature to state if the new COVID-19 cases are more severe as there is not much relevant data to analyze this although most of the 19,900 odd cases were identified in those that had bee hospitalized or were consulting doctors as a result of the symptoms.

This resurgence serves as a caution that variant evolution, and relaxed measures can allow periodic rebounds, emphasizing the need for continued vigilance, precautions, and monitoring to avert escalation.
 
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Milk Protein Shows Powerful Antiviral Potential
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 15, 2026

Scientists are increasingly investigating a natural protein found in milk that could help combat a wide range of viral diseases. Known as lactoferrin, this multifunctional protein has attracted global attention because of its ability to block viral infections, regulate immune responses, and reduce inflammation. Recent scientific findings suggest that lactoferrin may offer a promising supportive strategy in the fight against many viruses that threaten global health.

The research was conducted by scientists from the Laboratorio de Patología Molecular Veterinaria, Unidad de Investigación Multidisciplinaria, Facultad de Estudios Superiores Cuautitlán at the Universidad Nacional Autónoma de México in Cuautitlán Izcalli, Mexico; the Departamento de Biología Celular at the Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV-IPN) in Mexico City; and the Laboratorio 3, Unidad de Investigación Multidisciplinaria, Facultad de Estudios Superiores de Cuautitlán, Universidad Nacional Autónoma de México.


What Exactly Is Lactoferrin
Lactoferrin is a naturally occurring glycoprotein that forms part of the body’s innate immune system. It is present in many bodily fluids, including saliva, tears, and mucus, but it is especially abundant in breast milk, particularly in early milk known as colostrum. This protein plays a vital role in maintaining immune balance, regulating iron levels, and protecting the body from invading microbes.

Human milk contains especially high levels of lactoferrin during early lactation, reaching concentrations of more than five milligrams per milliliter in colostrum. Over time, the levels gradually decline but still remain an important component of breast milk that helps protect infants against infections.

Researchers believe that lactoferrin contributes significantly to the reduced rates of infections observed in breastfed infants, particularly infections affecting the digestive and respiratory systems.


How Lactoferrin Blocks Viruses
What makes lactoferrin particularly interesting to scientists is its ability to interfere with viral infections at multiple stages. Instead of targeting only one step of viral replication, the protein appears capable of blocking several key processes that viruses rely on to infect human cells.

One of the main mechanisms involves the ability of lactoferrin to attach to molecules on the surface of human cells called heparan sulfate proteoglycans. These molecules are commonly used by many viruses as docking points before entering cells. By binding to these receptors, lactoferrin effectively blocks viruses from attaching and penetrating the cell.

In addition to preventing viral attachment, lactoferrin can also bind directly to viral particles themselves. This interaction can neutralize the virus and stop it from initiating infection.

Laboratory studies have s hown that lactoferrin can inhibit a wide variety of viruses, including influenza viruses, herpes simplex virus, hepatitis viruses, respiratory syncytial virus, rotavirus, norovirus, and several human coronaviruses including SARS-CoV-2.


Evidence From Laboratory and Animal Studies
Experiments have demonstrated that lactoferrin can reduce viral infection rates significantly in cell cultures. In some studies involving arboviruses such as Zika and Chikungunya viruses, infection levels dropped by as much as 80 percent when lactoferrin was present.

Research in animal models has also revealed important immune-boosting effects. Oral administration of lactoferrin has been shown to increase the activity of natural killer cells and stimulate the production of immune signaling molecules such as interferons and interleukin-18. These molecules are essential for coordinating the body’s antiviral defenses.

The protein also appears to reduce harmful inflammation during infections, which is particularly important in viral diseases where excessive immune responses can worsen symptoms.

This Medical News report highlights how the protein’s unique ability to both block viruses and regulate immune responses has sparked interest in its potential medical applications.


What Clinical Trials Are Showing
Several clinical trials have examined the effects of lactoferrin in humans. In studies involving children with viral gastroenteritis caused by rotavirus, daily lactoferrin supplementation significantly reduced the duration and severity of symptoms such as diarrhea and vomiting. Children receiving lactoferrin were also less likely to experience dehydration severe enough to require hospitalization.

Other trials have evaluated lactoferrin for respiratory infections. In a clinical study involving COVID-19 patients treated with liposomal lactoferrin formulations, many participants experienced improvements in symptoms such as fatigue, cough, muscle pain, and headache within the first few days of treatment.

However, not all studies have produced consistent results. Some clinical trials found limited benefits when lactoferrin was administered later during illness, suggesting that the timing of treatment may be crucial for achieving the best results.


Conclusion
The growing body of research suggests that lactoferrin could play a valuable role as a supportive therapy against viral infections. By blocking viral entry into cells, interfering with viral replication, and strengthening immune defenses, this naturally occurring protein demonstrates a unique combination of protective mechanisms. While further large-scale clinical trials are still needed to confirm its full therapeutic potential, current evidence strongly supports continued investigation into lactoferrin as a safe and promising antiviral agent capable of helping the body defend itself against a wide spectrum of viral diseases.

The study findings were published in the peer reviewed journal: Future Pharmacology.
 
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Aged Care Home Fined $150,000 for COVID-Era Work Safe Breaches, Family Disappointed

A Victorian aged care facility, where 45 residents died from COVID-19 in 2020, has faced court.
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A Victorian court has sentenced St Basil’s Home for the Aged after an outbreak at the peak of the COVID-19 pandemic, which also led to the deaths of 45 residents in 2020.
Crystal-Rose Jones
3/15/2026 | Updated: 3/16/2026

St Basil’s was convicted and fined $150,000 for being aware of COVID-19 risks but not enforcing sufficient workplace measures. The fine was not over resident deaths, but rather for breaching workplace health and safety among a handful of staff members.

The court heard that in July 2020, there were approximately 92 residents and 106 staff at the workplace.

In January that same year, the World Health Organisation declared the COVID-19 pandemic a public health emergency of international concern.

Then, in March that year, the Communicable Diseases Network Australia published specific guidelines for management of the pandemic in residential care facilities.

Guidelines included identifying COVID-19 and its routes of transmission, identifying people at risk, stocking and use of personal protective gear, and ensuring staff are fully trained in outbreak management.

Later in March 2020, the Victorian government declared a state of emergency.

Before the court on March 11, 2026, the prosecution argued St Basil’s had failed to provide a safe working environment for some employees as stipulated by the guidelines.
It was stated that at least five employees were not adequately trained in safety measures, including wearing protective equipment.

The County Court of Victoria heard that St Basil’s not-for-profit organisation, operating under the auspice of the Greek Orthodox Archdiocese of Australia, has made strides to improve its operations.

At the time of the outbreak, the aged care home was still a fully paper-based facility but now has digital systems in place for better efficiency.

The not-for-profit company has also since established various systems for safety and compliance around disease outbreaks.

The defendant also told the court that a new structure had been developed and enhanced since the outbreak in 2020, to ensure that the failures identified in 2020 cannot occur under current governance.

In sentencing considerations, Judge Trevor Wraight found “there were weaknesses in the system, where five staff did not receive training, giving rise to the identified risks.”

In its mitigating factors regarding Basil’s, the court took into account an early guilty plea alongside acknowledgement that the facility had already suffered significant consequences through enormous public attention via the media.

Judge Wraight noted that without the plea of guilty from St Basil’s, the $150,000 fine would have amounted to $250,000.

Outside the court hearing, AAP reported the disappointment of families.

Spiros Vasiliakis, who also lost his mother Maria, said families had placed their trust in the provider to take care of their loved ones.

“They weren’t,” he said.

“In the most crucial time of their need to care, and a showing of duty of care, they completely dropped the ball.”
 
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This is a two-parter. Read this together with the next article and it starts to make sense....




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Inappropriate antibiotic use for COVID-19 is linked to resistance
by University of California, San Francisco
edited by Gaby Clark, reviewed by Robert Egan
March 16, 2026

Taking azithromycin for as little as one day triggers antibiotic resistance in the respiratory tract, according to a first-of-its kind look by scientists at UC San Francisco of the changes that occur in the microbiome of hospitalized patients who were treated for COVID-19. Azithromycin is one of the most widely used antibiotics in the world, and it is essential for treating certain classes of bacterial infections that cause strep throat, pneumonia, and sexually transmitted diseases. But it does not work against viruses.

Early in the pandemic, azithromycin was widely used after small studies suggested it might have therapeutic benefit. Randomized clinical trials later showed it did not work, but the drug continued to be prescribed to patients with respiratory illnesses.

"We've known for years that antibiotics don't treat viral infections, but these results were striking," said Chaz Langelier, MD, Ph.D. "That we could see resistance genes turning on in the respiratory tract within a day tells us the consequences of unnecessary antibiotic use aren't theoretical or long-term. They're immediate, measurable, and biologically real."

The results, published March 16 in Nature Microbiology, are from a multi-center genomic study.

Researchers followed 1,164 COVID-19 patients who had been hospitalized at more than 20 U.S. hospitals between May of 2020 and March of 2021, before COVID vaccines were widely available.

They compared the patients who were given azithromycin to those who received no antibiotics, as well as to patients who were given other antibiotics.

Azithromycin changed the mix of microbes in the upper airway. Some normally harmless bacteria decreased, while potentially harmful bacteria became more common. These changes persisted for more than a week.

Next, the researchers will look at whether other widely used antibiotics, such as amoxicillin and ceftriaxone, have similar effects in hospitalized patients.

Publication details
Abigail Glascock et al, Empiric azithromycin alters the upper respiratory microbiome and resistome without anti-inflammatory benefit in COVID-19, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02285-8
Journal information: Nature Microbiology
 
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Scientists Identify “Good” Bacteria That May Prevent Long COVID
By University of Louvain
March 21, 2026

A small microbe in the respiratory tract may hold important clues about why long COVID persists.

According to the WHO, about 6% of people worldwide who get COVID-19, roughly 400 million people, later develop a long-lasting form of the illness. That shows the condition remains a significant public health challenge.

In 2021, during the COVID-19 pandemic, the University of Louvain (UCLouvain, Belgium) and its hospital, the Cliniques universitaires Saint-Luc, launched a large-scale study to see whether long-term symptoms could be predicted during the acute phase of infection. The goal was to better understand the biological mechanisms involved and potentially identify a preventive treatment.

A Bacterium Linked to Recovery

After five years of research, scientists identified an important role for Dolosigranulum pigrum, a bacterium that naturally lives in the respiratory microbiome. Higher levels of this bacterium were associated with a lower likelihood that long Covid symptoms would persist.

Jean Cyr Yombi, Leïla Belkir, and Julien De Greef, UCLouvain professors and infectious disease specialists at the Cliniques universitaires Saint-Luc, examined the severity of long Covid symptoms in 156 patients. They focused mainly on severe fatigue, cognitive problems, and respiratory issues (shortness of breath).

Laure Elens and Patrice Cani, also UCLouvain professors, along with Bradley Ward, a postdoctoral researcher at the UCLouvain Louvain Drug Research Institute, then analyzed blood samples and nasopharyngeal swabs for molecular signatures linked to this more severe form of the disease. These signatures may help explain why symptoms persist in some patients but not in others.

Clues From the Respiratory Microbiome

UCLouvain and Cliniques universitaires Saint-Luc researchers stated, “This study suggests that certain so-called protective bacteria in the respiratory microbiome may be associated with improved recovery following viral respiratory infections (such as long Covid or influenza), and that their alteration (particularly in the context of severe infection or non-targeted antibiotic therapy) may influence longer-term clinical outcomes.”

In simpler terms, when this bacterium is present in higher amounts, it appears to help protect against long Covid or severe influenza (through a mechanism that has yet to be elucidated). When it is present at low levels, researchers found a greater tendency toward developing a persistent form of the disease.

Implications for Future Treatments

Researchers already knew this bacterium had a protective effect in infectious influenza. The new findings, published in Microbiology Spectrum, add to the evidence that Dolosigranulum pigrum may be beneficial.

Scientists hope the discovery will speed up research and support new treatment strategies, including the possible development of a probiotic, for example, in the form of a nasal spray, that could be used before winter to help protect people from severe infectious diseases such as Covid-19 or influenza.

The study also found that non-targeted antibiotics can affect the respiratory microbiome’s ability to defend against severe infections. That is another reason careful antibiotic use remains important.

Reference: “Association of nasopharyngeal Dolosigranulum pigrum and Corynebacterium species with post-acute sequelae of SARS-CoV-2 in a longitudinal cohort” by Bradley Ward, Laure B. Bindels, Jean-Luc Balligand, Bertrand Bearzatto, Guido Bommer, Patrice D. Cani, Julien De Greef, Joseph P. Dewulf, Laurent Gatto, Vincent Haufroid, Sébastien Jodogne, Benoît Kabamba, Sébastien Pyr dit Ruys, Didier Vertommen, Jean Cyr Yombi, Leïla Belkhir and Laure Elens, 17 March 2026, Microbiology Spectrum.
DOI: 10.1128/spectrum.02313-25

This research involved the University of Louvain HYGIEIA consortium and the Cliniques universitaires Saint-Luc, and was made possible thanks to the support of the Sofina Covid Solidarity Fund and partnerships with the Fondation Saint-Luc, the FNRS (via an emergency research grant) and the WEL Research Institute of the Walloon Region.
 
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New Evidence Shows COVID-19 Weakens Body’s Stress Hormone System
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 17, 2026

A new scientific investigation has revealed a surprising and potentially dangerous effect of COVID-19 on the human body—its ability to weaken the very hormonal system that normally helps control inflammation and stress. The findings shed light on why some patients struggle to recover and why inflammation can spiral out of control during infection.

Researchers from the Clinic of Endocrinology and Metabolic Diseases at University Hospital “Dr. G. Stranski” in Pleven, Bulgaria, the Department of Cardiology, Pulmonology, Endocrinology and Rheumatology at Medical University Pleven, the Biology Division at the Department of Anatomy, Histology, Cytology and Biology at Medical University Pleven, and the Clinical Laboratory Division at the Department of Clinical Immunology at Medical University Pleven conducted this important study involving 101 participants.


COVID-19 Disrupts the Body’s Hormone Balance
The study focused on cortisol, often called the “stress hormone,” which plays a key role in calming inflammation. Surprisingly, researchers found that about two-thirds of patients with active COVID-19 had unusually low cortisol levels.

This is alarming because during illness, the body normally increases cortisol production to fight inflammation. Instead, COVID-19 appears to interfere with this natural defense system. According to the data, patients with active infection had the lowest cortisol levels, while healthy individuals had the highest.

Even months after recovery, many individuals still showed reduced cortisol levels, suggesting that the virus may cause longer-term hormonal disruption.


A Hidden Problem: Hormone Resistance
Beyond low hormone levels, scientists discovered another critical issue—glucocorticoid resistance. This means that even when cortisol is present, the body may not respond to it properly.

This happens because of reduced levels of a key receptor called glucocorticoid receptor alpha (GRa), which allows cortisol to work inside cells. The study found that GRa levels were lowest during active infection, partially improved after recovery, but still did not return to normal.

This finding is crucial because it explains why inflammation can remain uncontrolled in COVID-19 patients, even when treatments are given.


Inflammation and Hormone Breakdown Are Linked
The research also examined inflammatory markers—chemical signals in the body that rise during infection. Three important ones were studied: IL-17A, TNF-alpha, and IL-10.

During active COVID-19, these markers were closely linked to changes in cortisol and GRa levels. This suggests a dangerous cycle: inflammation disrupts hormone signaling, and weak hormone signaling allows inflammation to worsen. Interestingly, these strong connections were only seen during active infection, highlighting how intense and uniq ue the body’s response to COVID-19 can be.


Why This Matters for Patients
This Medical News report highlights a key reason why some COVID-19 patients become severely ill. If the body cannot properly control inflammation due to hormone dysfunction, it can lead to complications affecting multiple organs.
The findings also suggest that simply measuring cortisol levels may not be enough. Doctors may need to consider how well the body is responding to cortisol, not just how much is present.


Key Study Findings
-Many COVID-19 patients have low stress hormone levels

-The body may also become resistant to these hormones

-This leads to poor control of inflammation

-Hormonal disruption may continue even after recovery

-The problem is strongest during active infection


Conclusion
The study clearly shows that COVID-19 does more than affect the lungs—it disrupts a critical hormonal system that helps regulate inflammation. This dual problem of low cortisol and reduced hormone sensitivity may explain severe disease and prolonged recovery in many patients. Understanding this mechanism could open the door to better treatments that target both inflammation and hormone function, potentially improving outcomes and saving lives in future outbreaks.

The study findings were published in the peer reviewed journal: COVID.
 
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COVID-19 Including Mild Infections, Raises the Risk of Infectious Mononucleosis
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 17, 2026

A large new study from Sweden has uncovered an alarming link between COVID-19 and a higher risk of developing infectious mononucleosis, a condition caused by the Epstein-Barr virus (EBV). What is particularly concerning is that even people with mild COVID-19 appear to face this increased risk, pointing to deeper and longer-lasting effects on the immune system.


Massive Population Study Reveals Hidden Risk
Researchers from Örebro University in Sweden, including Snieguole Vingeliene, Scott Montgomery, and Ayako Hiyoshi, carried out a nationwide study involving nearly 10 million individuals aged between 3 and 100 years. The study tracked participants from January 2020 to November 2022 using detailed national health records.

Participants were divided into three groups: those who never had COVID-19, those who tested positive but were not hospitalized, and those who required hospital care due to severe COVID-19. The researchers focused on cases of infectious mononucleosis severe enough to require hospital treatment. This illness, often referred to as glandular fever, is caused by EBV and is known for symptoms such as extreme fatigue, fever, sore throat, and swollen lymph nodes.


Strong Link Between COVID-19 and Later Illness
The results showed a clear and consistent pattern. People who had COVID-19 were more likely to later develop infectious mononucleosis compared to those who never had the virus.

Among individuals without COVID-19, about 4.6 cases per 100,000 people occurred annually. This increased to 7.8 per 100,000 among those who had mild COVID-19. For those hospitalized due to COVID-19, the rate rose to 10.5 per 100,000.

After adjusting for age, gender, region, and existing health conditions, the findings remained strong. Individuals with mild COVID-19 had a 61 percent higher risk, while those with severe COVID-19 had nearly six times the risk of developing infectious mononucleosis.

This Medical News report emphasizes that the consistency of these findings across different groups strengthens the evidence that COVID-19 plays a role in triggering this condition.


How COVID-19 Disrupts the Immune System
Scientists believe the connection lies in how COVID-19 affects the immune system. The virus is known to cause widespread inflammation and can leave lasting changes in immune function for months after infection.

Important immune markers such as interleukin-6 and tumor necrosis factor-alpha remain elevated, while key immune cells may not function normally. These changes can weaken the body’s ability to control other viruses already present in the body. EBV is one such virus. It infects more than 90 percent of people worldwide and remains dormant in the body for life. Under normal conditions, the immune system keeps it under control. However, COVID-19 may disturb this balance, allowing EBV to reactivate a nd cause infectious mononucleosis.


More Than Just a Temporary Illness
Although infectious mononucleosis is often seen as a short-term illness, it can have long-lasting effects. Many people experience extreme fatigue that can continue for months, affecting their ability to work or study. In some cases, EBV infection has been linked to serious long-term conditions, including multiple sclerosis, autoimmune diseases like lupus and rheumatoid arthritis, and certain cancers such as Hodgkin’s lymphoma.

The researchers caution that their study only included hospital-treated cases, meaning milder infections were not captured. This suggests the true number of cases could be much higher.


Younger Individuals May Be More Vulnerable
A notable finding was that many of those affected were relatively young. This raises concerns that COVID-19 may have a stronger impact on younger immune systems than previously believed.

While the overall risk of severe complications remains low, experts warn that the long-term effects of widespread EBV reactivation following COVID-19 are still unclear and may take years to fully understand.


Conclusions Highlight Long-Term Health Concerns
The findings strongly suggest that COVID-19 can leave lasting effects on the immune system, increasing vulnerability to other infections such as infectious mononucleosis. Even mild infections appear capable of triggering these changes, which may have broader implications for long-term health. This highlights the importance of continued research, monitoring, and awareness, as the full extent of post-COVID immune disruption and its potential role in future chronic diseases is only beginning to emerge.

The study findings were published in the peer reviewed journal: Clinical Infectious Diseases.
 
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CDC vaccine adviser Malone steps down to avoid 'drama'
Story by Ariel Cohen - Roll Call
March 24 2026

Robert Malone, an ideological ally of Health and Human Services Secretary Robert F. Kennedy Jr., is stepping away from the Centers for Disease Control and Prevention’s vaccine advisory committee following a court ruling that effectively nullified the panel.

Malone was one of several picks by Kennedy in a controversial reworking of the entire Advisory Committee on Immunization Practices last year. Malone said Tuesday that he won’t be a part of any attempt to reform the panel after a feud with HHS personnel on whether the court ruling would be appealed.

A federal judge last week blocked the vaccine panel’s controversial changes to the childhood vaccine schedule and called into question the panel’s validity, essentially kneecapping it from any future actions.

Malone posted on social media that the decision wouldn’t be appealed, which was contradicted by HHS spokeman Andrew Nixon.

“After Andrew trashing me with the press, I am done with the CDC and ACIP,” Malone said in a text message Tuesday morning. “That was the last straw.”

“Suffice to say I do not like drama, and have better things to do,” Malone added.

A physician and biochemist, Malone had questioned the severity of the COVID-19 pandemic and, according to FactCheck.org, elevated unfounded claims about the disease.

While on the panel, he supported more limited COVID-19 vaccine recommendation, arguing that Americans should be guided by consultations with health care providers rather than “propaganda, marketing and other activities that are not based in an actual, real world assessment of their risks and benefits.”

He was involved in some early research of mRNA technology and had earlier served in advisory roles for HHS and the Department of Defense, with expertise in molecular biology, immunology and vaccine development.

Malone’s departure represents the latest drama for the panel, which began last summer when Kennedy fired all 17 committee members and replaced them with handpicked ideological allies, many of whom are vaccine skeptics.

The committee made several major changes to the childhood vaccine schedule in recent months, including removing the recommendation for the birth-dose hepatitis B vaccine, rotavirus vaccine, annual flu shot and others. Before it was kneecapped by the courts, the committee planned to continue reevaluating that schedule, a priority for Kennedy and the “Make America Healthy Again” movement.

The CDC vaccine advisory is barred from convening until a decision is reached in the court case. The committee typically develops recommendations on the use of vaccines, including new flu shots and COVID-19 boosters, after Food and Drug Administration approval. New vaccines can still go into circulation without the CDC panel’s input.

The Trump administration faces a deadline to nominate a new CDC director this week.
 
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CDC raises alarm after new Covid variant from South Africa found in US

With detections increasing in recent months and the variant now present across multiple regions, experts at the CDC are watching to see whether it gains a stronger foothold in the US.
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CDC raises alarm after new Covid variant from South Africa is found in dozens of samples in US
Cassidy Morrison
25 March 2026

A new, highly mutated Covid variant is quietly spreading across the US, prompting the CDC to take notice.

The variant, known as BA.3.2, first appeared in South Africa in November 2024 and scientists are concerned that it could be significantly more adept at sidestepping immune defenses, particularly the protection provided by the 2025-2026 Covid vaccines.

The variant’s spike protein, which vaccines train the body to recognize and fight, has undergone about 75 mutations. That makes it look like an entirely new threat to the immune system compared to other recent strains.

As of mid-March 2026, BA.3.2 has turned up in six travelers, three airplane wastewater samples, over two dozen patients and 260 wastewater sites across 29 states and Puerto Rico. Overall, it accounts for a small fraction, about half a percent, of recent virus sequences, according to the latest CDC data.

Wastewater surveillance is often the first clue that a virus is gaining a foothold in the community. In this case, it detected BA.3.2 weeks before doctors saw it in patients.

Detections of BA.3.2 started climbing in Europe last fall, reaching roughly 30 percent of cases in Denmark, Germany, and the Netherlands. It has not yet taken over in the US, but its ability to spread alongside other more dominant variants suggests it has been mutating for a while.

Two lab studies found that BA.3.2 does not bind as well to human cells as other variants do, and that weakness may be holding it back from spreading faster.

The CDC is monitoring the spread of BA.3.2 by testing international travelers, sampling airplane wastewater and monitoring sewers nationwide. These systems captured the variant’s arrival in the US in June 2025, months before it appeared in hospitals.

While BA.3.2 may be better at evading immunity, the current vaccines still offer protection against severe disease.

BA.3.2 was first detected in a five-year-old boy in South Africa in November 2024. It then appeared in Mozambique and a few European countries in early 2025.

Detections were sparse at first but began climbing that September, peaking in December.

BA.3.2 first reached the US on June 27, 2025, when a traveler flying from the Netherlands tested positive at San Francisco International Airport.

Reports started ticking up in September 2025, but because many countries lack the sophisticated surveillance tools necessary to closely track variants, ‘these detections likely underrepresent the actual geographic extent of spread,’ according to the CDC.

Wastewater surveillance in the US picked it up in Rhode Island that November, months before clinical cases appeared.

The first patients were reported in early January 2026 — two older hospitalized adults with underlying conditions and a young child. All of them survived.

By February 2026, BA.3.2 had appeared in a handful of international travelers, a few clinical patients and over 130 wastewater samples across two dozen states.

To track Covid variants, the CDC pulls data from three main sources: national lab testing, travelers arriving at airports, including volunteer nasal swabs and airplane wastewater, and a nationwide wastewater surveillance system that monitors about 1,450 sewer sites.

When scientists find a BA.3.2 sample, they analyze its genetic code, comparing it to current vaccines to see what has changed. They use software to line up sequences side by side, building family trees that show how different versions are related.

Every detection is logged by location and date, allowing the CDC to map where it first appeared and how quickly it moves, giving officials a real-time view of the evolving variant.

According to the agency, BA.3.2 is genetically distinct from the JN.1 family of variants that have dominated in the US since early 2024.

Compared to the strain used in current vaccines, BA.3.2 has about 70 to 75 mutations on its spike protein.

Of those, 20 are in the part that grabs onto human cells, 35 are in a nearby region that also helps the virus infect cells and evade immunity and the remaining changes are scattered elsewhere on the spike.

The current Covid vaccine, updated for the 2025–26 season, works well against the dominant JN.1 strains still circulating.

In a lab study comparing seven variants, it performed worst against BA.3.2. That means the vaccine may offer less protection against this particular variant, though real-world data is still needed to know for sure.

Covid has gone from being a consistent viral threat to a seasonal public health concern alongside the flu and respiratory syncytial virus (RSV).

In 2020 and 2021, the country would often experience waves of such severe disease transmission that thousands of patients were dying each day.

Now, the virus follows a predictable seasonal rhythm with far shorter peaks thanks to highly effective vaccines and the antiviral drug Paxlovid.

Like the flu, Covid now tends to spike during the colder months, from late fall through early spring, when people gather indoors and the virus spreads more easily. In the summer, cases typically drop.

Most of the population now has some protection from a combination of vaccination, prior infection, or both. That does not stop everyone from getting sick, but it does mean most people who catch it will not end up in the hospital.
 
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Why the current ‘calm’ in SARS-CoV-2 evolution is an illusion of stability (‘endemicity’) and actually signals growing instability

You Can Lock Down Society But Not Viral Evolution in Highly Covid-19-Vaccinated Populations!
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Why the current ‘calm’ in SARS-CoV-2 evolution is an illusion of stability (‘endemicity’) and actually signals growing instability
You Can Lock Down Society But Not Viral Evolution in Highly Covid-19-Vaccinated Populations!
Geert Vanden Bossche
Mar 24, 2026

A new SARS-CoV-2 (SC-2) variant called BA.3.2 has attracted attention for several months now. At first glance, it might look like just another addition to the long list of Omicron subvariants. But a closer look suggests that something more fundamental may be unfolding.

BA.3.2 is not a typical variant. It carries a very large number of mutations, particularly in the spike (S) protein-the primary target of the immune response following natural infection and the target antigen used in all current COVID-19 (C-19) vaccines. In simple terms, it looks like the virus has made a large evolutionary jump (so-called ‘saltatory evolution’) rather than gradual step-by-step changes.

Scientists such as Kei Sato and colleagues have pointed out that BA.3.2 seems particularly good at evading antibodies (as reported on X by The Sato Lab). That is already notable. But what makes the situation more interesting is what happens next. Despite all these changes, BA.3.2 has not taken over.

As observed and reported on X by mutation spotters such as R. Hisner, the variant does not spread like a clearly ‘better’ virus would. Instead, it competes with other variants, rises somewhat in some places, and then levels off or declines (as reported on X by S. Pöhlmann, based on multiple independent tracking analyses across different countries). In other words, it behaves indecisively.

A Strange Pattern

Normally, when a virus evolves a major advantage, one of two things happens:

- it spreads quickly and replaces other variants or

- it disappears because the changes come at a significant fitness cost

BA.3.2 does neither. It persists, but without clearly winning. This is unusual and scientifically highly informative. It suggests that the virus may no longer be evolving freely. Instead, it may be running into increasing immunological and structural constraints as explained in several of my previous Substack articles.

What Changed?

Earlier in the pandemic, the virus mainly evolved to spread faster. Any mutation that improved transmission had a clear advantage. This became particularly pronounced once large parts of populations became vaccinated and immune escape variants-culminating in Omicron-were selected under population-level immune pressure.

Today, the situation is very different. Highly C-19-vaccinated populations now have some level of collective immunity, although suboptimal and narrowly focused, especially against the S protein. This creates strong immune pressure on the S protein, which is largely responsible for viral entry and infectivity.

At first, the virus readily escaped from this pressure by changing those S-associated targets, a phenomenon often referred to as immune refocusing, where the adaptive immune response is redirected toward alternative, often less immunogenic and more conserved epitopes on S protein. But over time, a problem arises as I already described in a series of previous Substack articles:

i) many of the most relevant immune targets have already been altered

ii) new mutations provide diminishing returns because functional and spatial constraints increasingly limit viability of additional S-based mutations

iii) earlier escape mutations cannot be reversed without restoring immune sensitivity and losing fitness advantage

The result is that the virus becomes trapped in a narrowing evolutionary corridor.

Why This Matters

In such a situation, even large changes-like those seen in BA.3.2-may no longer lead to clear evolutionary success. That is exactly what we are observing. BA.3.2 (sub)lineages are characterized by:

a) a high number of mutations

b) strong immune escape properties

c) lack of clear epidemiological dominance

This combination suggests that additional immune escape mutations no longer translate into decisive competitive advantage.

In other words, immune-driven selection pressure appears to be reaching functional limits in its ability to select variants that clearly outcompete others.

Ongoing Spread Keeps the System Active in Highly C-19-vaccinated Populations

Another key point is that the virus is still spreading widely.

Even though severe disease is less common, the virus still spreads widely: many infections are mild or even unnoticed, allowing the virus to circulate easily. In addition, some people develop chronic infection and carry the virus for longer periods, thereby contributing to extended viral shedding and giving it more time to evolve.

As long as the virus continues to replicate at scale, it keeps exploring new mutations even if a shift in predominance from immune pressure–driven selection to fitness-driven selection slows down viral evolutionary dynamics.

This matters because evolution depends on numbers:

i) more infections and/or prolonged transmission periods entail more replication
ii) more replication causes more mutations
iii) more mutations increase the probability of a newly emerging lineage capable of
breaking through the entire immune system

Hence, as long as the infectious viral burden remains sufficiently elevated in highly C-19-vaccinated populations, the virus continues to generate and test new configurations within a constrained fitness landscape.

No Endemicity But An Unstable Situation

What we are seeing now is not a stable endpoint and therefore not consistent with what our public health authorities and so-called ‘experts’ are trying to make people believe, namely that the virus has simply transitioned into a benign endemic phase!

Instead, it resembles a system under pressure because

i) the virus continues to replicate and change (as reflected by wastewater surveillance
samples)

ii) but gains are limited and inconsistent/ fluctuating

iii) variants compete, yet no single variant clearly dominates

This type of situation can persist for some time, but it reflects dynamic instability rather than equilibrium. Small changes in viral properties, the population’s immune background or socio-environmental determinants can lead to noticeable fluctuations in the prevalence of BA.3.2 or other co-circulating variants in highly C-19-vaccinated populations.

This persistent reshuffling of variant proportions is itself a hallmark of a metastable system. But it usually does not last forever because new mutations have less and less functional impact and old changes cannot be undone.

Together, this suggests that the virus is not settling into stability-it continues to experience additional immune pressure (albeit weaker) and to evolve (albeit less efficiently) while still searching for a way to adapt to the hostile immune environment of highly C-19-vaccinated populations (albeit at a much slower pace).

What appears as ‘calm’ may actually reflect a system under tension

Although this system can persist for a while, such unstable balances in complex systems often end not gradually, but suddenly, i.e., when changes accumulate sufficiently to push the system past a tipping point, triggering a phase transition.

What About the United States?

The U.S. adds an important piece to the puzzle.

Although BA.3.2 has been detected in some clinical and wastewater surveillance samples from multiple states, it currently plays no significant role in the U.S. SC-2 landscape. Yet the same overall pattern is observed: multiple variants continuously rise and fall in relative proportion, without any single lineage establishing long-term dominance (see figure below).

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This is important as it indicates that the underlying phenomenon is not specific to BA.3.2.

Whether BA.3.2 will become more prevalent in the US or not remains uncertain but this does not change the overall observation that the virus as a whole is in a state where it keeps evolving while no variant clearly dominates. Hence, even in the absence of significant BA.3.2. co-circulation, the virus appears to be evolving within constraints, without reaching a stable solution. Hence, the presence of BA.3.2 is not required to demonstrate that the system itself is metastable and unresolved.

What Could Happen Next?

If current conditions persist-ongoing transmission combined with a constrained evolutionary landscape-the probability increases that a new variant with a markedly different antigenic and/or functional profile, enabling a much stronger competitive advantage, could emerge.

However, because the virus is operating under decreased additional immune pressure and within a restricted evolutionary space, it may take time for such a variant to arise. In order for a new viral lineage to acquire a truly significant fitness advantage, it would likely need to overcome existing adaptive immune memory while also effectively exploiting early infection dynamics.

As highly C-19-vaccinated populations are characterized by suboptimal adaptive immune responses and insufficiently trained cell-based innate immunity, they constitute an excellent breeding ground for such a lineage.

Such development would represent a qualitative shift in virus-host interaction, rather than a simple continuation of current trends.

It is difficult to envisage how such a qualitative shift could enable the virus to overcome the overall host immune response and maintain infectivity without becoming highly virulent.

This is where I anticipate the chronic phase of this immune escape pandemic to transition into a hyperacute phase, driven by a late, highly virulent Omicron descendant (HI-VI-CRON).

However, as the transition to a lineage that spreads very efficiently and outcompetes all other circulating variants may require some lag time, the emergence of HI-VI-CRON is unlikely to occur overnight (i.e., within a single day).

But let us be clear: this does not mean that the current situation should be mistaken for stability.

In Summary

BA.3.2 is unlikely to evolve consistently into the next dominant variant. But, together with the persistent fluctuations in co-circulating variants, it significance as a warning signal could be much more relevant than its epidemiological or clinical impact:

A signal that viral evolution is no longer evolving in a simple, predictable way as driven by selective immune pressure on S-associated B and Tc epitopes.

A signal that current immune and transmission dynamics are constraining viral adaptation in highly C-19-vaccinated populations.

A signal that the system is becoming unstable rather than settling down.

What looks like calm is, in reality, a system under pressure, still searching for a viable evolutionary path forward. As the current evolutionary dynamics suggest that continued instability is far more plausible than smooth resolution, the question doesn’t seem to be whether such a path will emerge but rather when it will do so.
 
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Hidden COVID-19 Deaths During the Early Pandemic Shocks America
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 19, 2026

Medical News: A startling new study suggests that the true death toll from COVID-19 in the United States during the early phase of the pandemic was far higher than official records indicated. Researchers now estimate that more than 150,000 additional deaths may have gone uncounted between 2020 and 2021, raising serious concerns about how the crisis was measured and understood.


A Bigger Death Toll Than Reported
Official figures show that around 840,000 Americans died from COVID-19 during the first two years of the pandemic. However, this new research indicates the actual number could be closer to one million when previously unrecognized deaths are included. That means roughly 16 to 19 percent of COVID-related deaths may not have been properly recorded.

The study was conducted by researchers from the University of Minnesota, Boston University, and collaborating institutions across the United States. Their findings point to a major gap in how deaths were tracked, especially outside hospitals.


Why So Many Deaths Were Missed
One key reason for the undercount is that many people died at home or in community settings without ever being tested for COVID-19. In the early months of the pandemic, testing was limited and often unavailable, particularly outside major hospitals.

To uncover hidden deaths, the researchers used advanced machine learning techniques. They trained artificial intelligence models using confirmed COVID-19 hospital death records and then applied those patterns to analyze deaths that occurred outside hospitals. Many of these deaths had been officially attributed to conditions such as pneumonia or diabetes, but the patterns suggested COVID-19 was likely involved.

This Medical News report highlights that early testing gaps and inconsistent death investigations played a major role in masking the true impact of the virus.


Inequality at the Heart of the Undercount
Perhaps most concerning is that the missing deaths were not evenly distributed. The study found that undercounted deaths were significantly more common among vulnerable populations, including Hispanic, Black, Asian, American Indian, and Alaska Native communities.

People with lower levels of education and those living in poorer counties were also more likely to have their deaths misclassified. Geographic disparities were clear as well, with states in the South and Southwest, such as Alabama, Oklahoma, and South Carolina, showing higher levels of underreporting. These patterns suggest that social and economic inequalities, along with limited access to healthcare, played a major role in who was counted and who was not.


Flaws in the Death Reporting System
The study also points to structural weaknesses in the U.S. death investigation system. In many areas, especially rural regions, death investigations ar e handled by elected coroners who may lack medical training. This can lead to inconsistent or inaccurate cause-of-death reporting.

Political attitudes and stigma around COVID-19 may have also influenced whether individuals sought testing or whether families agreed to list COVID-19 as a cause of death. In some cases, overwhelmed health systems and limited resources further complicated accurate reporting.


Why Accurate Data Matters
Accurate death counts are not just numbers. They guide public health decisions, funding, and emergency responses. When deaths are undercounted, communities most at risk may not receive the support they need. The study emphasizes that incomplete data may have weakened the overall pandemic response and hidden the true scale of health inequalities in the United States.


Conclusion
The findings reveal that the COVID-19 pandemic was even more devastating than previously believed, particularly for marginalized communities. The undercounting of deaths highlights serious gaps in healthcare access, testing availability, and death reporting systems. Addressing these weaknesses is critical, not only to ensure fairness and accuracy but also to better prepare for future public health emergencies and protect vulnerable populations more effectively.’

The study findings were published in the peer reviewed journal: Science Advances.
 
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Why the early U.S. COVID-19 death toll may be 155,000 higher
by Mike Stobbe
edited by Andrew Zinin
March 18, 2026

The COVID-19 pandemic's early death toll was much higher than the official U.S. count, according to a new study that spotlights dramatic disparities in the uncounted deaths.

About 840,000 COVID-19 deaths were reported on death certificates in 2020 and 2021. But a group of researchers—using a form of artificial intelligence—estimate that as many as 155,000 unrecognized additional deaths likely occurred in that time outside of hospitals. That would mean about 16% of COVID-19 deaths went uncounted in those years.

The overall findings, published Wednesday by the journal Science Advances, were close to estimates from other studies of pandemic deaths during that time. But the authors of the new study tried to determine exactly which deaths were more likely to be missing from the official tallies.

The answer: The undiagnosed dead were more likely to be Hispanic people and other people of color, who had died in the first few months of the pandemic, and who had been in certain states in the South and Southwest—including Alabama, Oklahoma and South Carolina.

Six years after the coronavirus swept through the U.S., barriers remain for many of the same people, said Steven Woolf, a Virginia Commonwealth University researcher not involved in the study.

"People on the margins continue to die at disproportionate rates because they can't access care," he said in an email.


Access to care wasn't the only challenge

While hospital patients were routinely tested for COVID-19, many who grew sick and died outside of hospitals were not tested—often because at-home testing was not readily available early in the pandemic, said one of the study's authors, the University of Minnesota's Elizabeth Wrigley-Field.

In some parts of the country, death investigations are handled by elected coroners who don't necessarily have the specialized training that medical examiners do. Some research has suggested partisan opinions could affect whether a sick person or their family members sought COVID-19 testing, and whether coroners pursued postmortem coronavirus testing. Indeed, some coroners said families had pressed them not to list COVID-19 as a cause of death.

"Our antiquated death investigation system is one key reason why we fell short of accurate counts, particularly outside of big metropolitan areas," said Andrew Stokes of Boston University, the senior author on the paper.


Death counts were swept up in COVID politics

The Centers for Disease Control and Prevention data count more than 1.2 million COVID-19 deaths since the pandemic erupted in early 2020. More than two-thirds of those reported deaths occurred in 2020 and 2021.

The count has long been debated, as false claims on social media said the number of COVID-19 deaths was inflated. Adding to the rancor was President Donald Trump, who in August 2020 retweeted a post claiming only 6% of reported deaths were actually from COVID-19—a post Twitter later removed.

To be sure, there were other kinds of pandemic deaths. For example, uninfected people died from other medical conditions because they could not get care at hospitals overloaded with COVID-19 patients. People with drug addictions died of overdoses as a result of social isolation and losing access to treatment. Other studies that have estimated the actual number of pandemic deaths have taken those deaths into account.

But Stokes and his collaborators wanted to focus on the deaths of people infected by the coronavirus. They used machine learning to sift through the death certificates of infected patients who died in hospitals and then used patterns observed in those records to evaluate death certificates of people who died outside hospitals and whose deaths were attributed to things like pneumonia or diabetes.

Scientists' understanding of the strengths and weaknesses of machine learning-reliant research is still evolving, but Woolf called this team's use of it "intriguing."


Publication details
Mathew Kiang et al, Applying Machine Learning to Identify Unrecognized COVID-19 Deaths Recorded as Other Causes of Death in the United States, Science Advances (2026). DOI: 10.1126/sciadv.aef5697. www.science.org/doi/10.1126/sciadv.aef5697
Journal information: Science Advances
 
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CDC raises alarm after new Covid variant from South Africa is found in dozens of samples in US
Cassidy Morrison
25 March 2026

A new, highly mutated Covid variant is quietly spreading across the US, prompting the CDC to take notice.

The variant, known as BA.3.2, first appeared in South Africa in November 2024 and scientists are concerned that it could be significantly more adept at sidestepping immune defenses, particularly the protection provided by the 2025-2026 Covid vaccines.

The variant’s spike protein, which vaccines train the body to recognize and fight, has undergone about 75 mutations. That makes it look like an entirely new threat to the immune system compared to other recent strains.
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New COVID 'Cicada' variant is spreading—what experts want you to know
by HealthDay Staff
edited by Gaby Clark, reviewed by Andrew Zinin
March 27, 2026

Another new COVID variant is starting to spread. Health officials say the variant—known as BA.3.2 or "Cicada"—has been quietly circulating for years but is now being detected more often in the United States and around the world.

The U.S. Centers for Disease Control and Prevention (CDC) said in a March 19 report that cases are slowly increasing. The World Health Organization (WHO) has also added Cicada to its "variants of monitoring" list as it pops up in more countries, U.S. Today reported.

So far, BA.3.2 has been found in more than 20 countries. In some places, it makes up as much as 30% of cases.

"Monitoring the spread of BA.3.2 provides valuable information about the potential for this new SARS-CoV-2 lineage to evade immunity from a previous infection or vaccination," the CDC wrote in its Morbidity and Mortality Weekly Report.

The variant was named after a breed of insects that rarely emerge into view because it stayed mostly "underground" once it was detected.

Dr. Robert Hopkins Jr., medical director of the National Foundation for Infectious Diseases, said the variant was first identified in a traveler coming to the United States in June 2025. The first U.S. case was reported in January.

Since then, Cicada has been found in wastewater samples from 132 locations across at least 25 states.

Globally, the first known case was in South Africa in November 2024. The uptick began in September 2025.

BA.3.2 stands out because it contains about 70 to 75 mutations, making it different from previous strains.

As of March 14, the variant made up about 3.7% of wastewater samples collected, according to tracking data. Another variant, XFG, remains most dominant at 53%, followed by LF.7 at 10.3%, U.S. Today said.

But the Cicada version has spread more widely in parts of Europe.

"It is possible we will see Cicada become the dominant strain in the U.S., but that is by no means certain," Hopkins told U.S. Today, adding that he is aware of concerns that it could drive a U.S. summer surge.

"Low vaccination rates and little to no public health effort toward stopping COVID infections and spread leaves us vulnerable," he said.

So far, symptoms appear to be similar to other COVID strains.

Those include:
  • Runny or stuffy nose
  • Headache
  • Fatigue
  • Sneezing
  • Sore throat
  • Coughing
  • Changes in taste or smell
Some people have also reported a very painful sore throat, sometimes called "razorblade throat."

"I have not seen any data which indicates that Cicada is any more severe than other circulating variants," Hopkins said.

In its report, the CDC said monitoring spread of the BA.3.2 variant provides "valuable information" about its potential to evade immunity provided by previous vaccination or infection.

"The number of mutations from JN.1 viruses makes it less likely that the current vaccines will be highly effective against Cicada, but we need more data to better answer this question," Hopkins said.

Nonetheless, vaccines should still help protect against severe illness and death. Taking some simple steps can also help reduce any risk:
  • Stay home if you're sick.
  • Improve ventilation at home.
  • Wear a high-quality mask if needed.
  • Keep up with vaccines and boosters.
  • Get tested if you have symptoms.
  • Talk to your doctor if symptoms worsen.
  • Get a lot of rest.
  • Use over-the-counter medications to manage symptoms.

Publication details
Mila Shakya et al, Early Detection and Surveillance of the SARS-CoV-2 Variant BA.3.2 — Worldwide, November 2024–February 2026, MMWR. Morbidity and Mortality Weekly Report (2026). DOI: 10.15585/mmwr.mm7510a1
The U.S. Centers for Disease Control and Prevention is tracking the new variant regularly.
Journal information: Morbidity and Mortality Weekly Report
 
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COVID-19 Linked Testicular Damage Shocks Doctors
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 19, 2026

A newly documented medical case is raising serious concerns about how COVID-19 may silently affect male fertility, even in men who never showed symptoms. Doctors have reported a rare but alarming situation where a previously healthy man developed complete testicular failure after what appears to be an unnoticed SARS-CoV-2 infection.


A Sudden and Rapid Decline in Fertility
The case involves a 40-year-old man who initially had only mild fertility issues. Early tests showed slightly reduced sperm movement and count. However, within just a few months, his condition rapidly worsened. His sperm count dropped dramatically from millions to almost zero, eventually reaching complete absence of sperm, a condition known as azoospermia.

Doctors were alarmed by how quickly this decline occurred. Even attempts to preserve fertility through sperm freezing yielded only a very small number of viable sperm cells.

This sharp deterioration suggested something more aggressive than typical infertility causes.


Hidden Infection Triggers Immune Attack
Further investigations revealed something unexpected. Although the patient had no symptoms and had not been recently vaccinated, blood tests showed extremely high levels of antibodies against SARS-CoV-2. This indicated a recent, likely unnoticed COVID-19 infection.

What makes this case unique is how the body responded. Instead of simply clearing the virus, the immune system appeared to mistakenly attack the testes. Tissue analysis showed clear signs of immune cells, particularly T-cells, invading the testicular tissue. These immune cells are usually meant to fight infections but, in this case, they caused inflammation and damage to sperm-producing structures.


Genetic Vulnerability Made Things Worse
Doctors also discovered that the patient had a rare genetic condition known as a balanced chromosomal translocation involving chromosomes 2 and 8. While this condition can sometimes affect fertility, it usually does not lead to such rapid and complete failure.

Experts believe this genetic issue made the testes more vulnerable.

When combined with the immune response triggered by COVID-19, it created what researchers describe as a “second-hit” effect. In simple terms, the virus may have acted as the tipping point that accelerated damage in an already sensitive system.


What The Tissue Findings Revealed
Detailed examination of testicular tissue showed severe damage. The sperm-producing cells were largely absent, and only a few immature cells remained. At the same time, immune cells were actively present, confirming ongoing inflammation.

Hormone tests further supported the diagnosis. Levels of key reproductive hormones such as luteinizing hormone and follicle-stimulating hormone were abnormally high, a sign that the body was trying, unsuccessfully, to stimulate failing testes.


Urgent Need fo r Awareness and Early Action
This Medical News report highlights the importance of early fertility evaluation in men experiencing sudden changes. Doctors stress that men planning to have children should seek medical advice quickly if they notice fertility issues, especially after COVID-19 exposure.

The case also underscores the importance of sperm preservation. In this situation, early intervention allowed at least some sperm to be saved for future assisted reproduction.


Conclusion
This case provides a striking example of how COVID-19 may trigger severe and irreversible reproductive damage in rare situations, particularly in individuals with underlying genetic vulnerabilities. While such outcomes appear uncommon, the speed and severity of the damage emphasize the need for awareness, early testing, and proactive fertility preservation. More research is urgently needed to understand how viral infections interact with the immune system and reproductive health, and to identify those at highest risk before permanent damage occurs.

The study findings were published in the peer reviewed journal: Cureus.
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Immune-Mediated SARS-CoV-2-Induced Orchitis Leading to Complete Testicular Failure: A Report of a Rare Case

Autoimmune orchitis is a rare cause of male infertility characterized by immune-mediated impairment of spermatogenesis. SARS-CoV-2 infection has been implicated in testicular inflammation and immune dysregulation, but reports of virus-associated autoimmune orchitis remain exceedingly uncommon...
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Herbal Breakthrough Slows Deadly Lung Inflammation
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 22, 2026

A team of researchers from the College of Chinese Materia Medica, Chongqing University of Chinese Medicine, the College of Traditional Chinese Medicine, Chongqing Medical University, and the Institute of Pharmacology and Toxicology, Chongqing Academy of Chinese Materia Medica have uncovered promising evidence that a traditional herbal remedy may help control life-threatening lung inflammation linked to sepsis and viral infections.

This Medical News report highlights how the plant Eupatorium lindleyanum DC. could play a crucial role in calming the dangerous immune overreaction known as a “cytokine storm,” a condition often seen in severe infections including COVID-19.


What Makes Cytokine Storms So Dangerous
When the body fights infection, it releases proteins called cytokines to help coordinate the immune response. However, in severe cases, this process goes into overdrive, flooding the body with excessive inflammatory signals. This “cytokine storm” can damage organs, especially the lungs, leading to breathing failure and even death.

The researchers focused on this problem because both sepsis and viral infections like COVID-19 share this same harmful mechanism. Finding a treatment that can safely calm this response could save many lives.


The Herbal Candidate Under Study
Eupatorium lindleyanum DC., a plant long used in traditional Chinese medicine, is known for its anti-inflammatory and antiviral properties. However, until now, scientists had not fully understood how it works inside the body.

The research team used a combination of laboratory experiments, animal studies, and computer simulations to explore its effects in detail. They identified 32 active compounds within the plant, many of which interact with key biological pathways linked to inflammation.


Key Findings from the Study
The results were striking. In animal models with severe lung injury, the herbal extract significantly reduced swelling, bleeding, and immune cell buildup in lung tissue. According to findings shown in lung tissue analysis, treated subjects had visibly healthier lung structures compared to untreated ones.

The herb also lowered levels of major inflammatory molecules such as TNF-a and IL-6—two of the main drivers of cytokine storms. Importantly, these reductions were dose-dependent, meaning higher doses led to stronger effects.

In cell-based experiments, the extract successfully blocked inflammatory signaling pathways, particularly NF-?B and PI3K–Akt. These pathways are known to act like “on switches” for inflammation. By turning them down, the herb effectively reduced excessive immune activity.


A Powerful Compound Called Hyperoside
One standout compound identified in the pl ant is hyperoside. The study showed that it binds strongly to key proteins involved in inflammation and viral infection, including ACE2—the receptor used by SARS-CoV-2 to enter cells.

In further experiments, hyperoside reduced lung damage in mice exposed to a coronavirus-like pseudovirus. It also lowered ACE2 levels and suppressed genes linked to inflammation, suggesting both anti-inflammatory and antiviral potential.


Why This Discovery Matters
These findings suggest that Eupatorium lindleyanum DC. works through multiple pathways at once. Instead of targeting just one part of the disease process, it acts broadly—reducing inflammation, protecting lung tissue, and potentially interfering with viral activity.


Conclusion
The study provides strong evidence that this traditional herbal medicine could offer a new approach to treating severe lung inflammation caused by infections. By targeting multiple biological pathways simultaneously, it may help control cytokine storms more effectively than single-target drugs. While further clinical studies in humans are needed, the results are highly encouraging and point toward a future where natural compounds could complement modern treatments in managing life-threatening inflammatory conditions.

The study findings were published in the peer reviewed journal: Current Issues in Molecular Biology.
 
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Why Aging Lungs Turn Mild Infections Into Life-Threatening Illness
By University of California - San Francisco
March 27, 2026

Aging lungs may be sabotaging themselves—fueling runaway inflammation that turns mild infections into life-threatening illness.

Older adults face a much higher risk of severe illness from flu or COVID, and new research from UC San Francisco points to a key reason. Aging lung cells appear to trigger overly strong immune reactions, which can turn even mild infections into serious health threats.

These findings shed light on the chronic inflammation linked to aging and help explain why something as simple as a cough can escalate into a hospital visit for older individuals.


Aging Lung Cells and Excessive Immune Response

To investigate what changes in older lungs, researchers altered fibroblasts, the structural cells that help support lung tissue, in young mice. They activated a distress signal typically associated with aging. This caused the lungs to develop clusters of inflamed cells, including some carrying the GZMK gene, which has previously been linked to severe COVID-19. Scientists believe future treatments could focus on these cells to interrupt the harmful cycle known as inflammaging.

“We were surprised to see lung fibroblasts working hand-in-hand with immune cells to drive inflammaging,” said Tien Peng, MD, a professor of Medicine and a member of the Cardiovascular Research Institute and Bakar Aging Research Institute at UCSF. “It suggests new ways to intervene before patients progress to severe inflammation that can require intubation.”

Peng is the senior author of the study, which was published in Immunity today (March 27). Nancy Allen MD, PhD, a clinical fellow in the Pulmonary and Critical Care Division in the UCSF Department of Medicine, is the first author.


Fibroblasts and the NF-kB Inflammation Pathway

Fibroblasts play an essential role in maintaining the structure of the lungs, keeping airways intact and functional. However, they are also known to contribute to inflammation in conditions such as COPD. The researchers set out to determine whether signals from these cells could disrupt otherwise healthy lung tissue.

They focused on a signaling pathway called NF-kB, which is commonly associated with age-related diseases. When activated, fibroblasts stimulated macrophages in the lungs to initiate an immune response. This, in turn, drew additional immune cells from the bloodstream, including those marked by GZMK.

Although GZMK-positive cells did not effectively fight infection, they still caused damage to lung tissue.
Immune Cell Clusters and Severe Lung Damage

After these inflammatory clusters formed, the young mice began to show severe symptoms when infected, resembling the response seen in older individuals. When researchers used a genetic approach to remove the GZMK cells, the mice were better able to tolerate the infection.

This points to a key conclusion: aging lung tissue itself may be a driving force behind harmful inflammation.

The team also analyzed lung samples from older patients hospitalized with COVID-related ARDS (acute respiratory distress syndrome). These samples contained similar clusters of inflamed cells to those observed in the mice. Patients with more severe illness had larger numbers of these clusters, while healthy donor lungs showed none.

“We saw during COVID that our most vulnerable patients no longer had the infection but still had persistent and devastating lung inflammation,” Peng said. “This circuit of dysfunction between lung and immune cells makes for a promising new therapeutic target.”

Reference: 27 March 2026, Immunity.

Other UCSF authors are Christian Ringler; Sang Ho Woo, PhD; Sophie Phipps; Jin Young Lee, PhD; Nabora Reyes, PhD; Ritusree Biswas, PhD; Lucile Neyton, PhD; Andrew Willmore; Sofia Caryotakis; Jessica Roginsky, PhD; Lu Guo; Melia Magnen, PhD; Chaz Langelier, MD, PhD; COMET Consortium; Mark Looney, MD; Averil Ma, MD; Vincent Auyeung, MD, PhD; Carolyn Calfee, MD; and Ari B. Molofsky, MD, PhD; as well as Pedro Ruivo of UC Davis.

This work was supported by the National Institutes of Health (P30DK063720, R01HL160895, F32HL156452, K08HL169723) and the Bakar Aging Research Institute.
 
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A New, Highly Mutated COVID Variant Called 'Cicada' Is Spreading in the US. Know These Symptoms

The heavily mutated new BA.3.2 COVID-19 variant, aka "cicada," is circulating in at least 25 U.S. states, the CDC said. What to know about its spread and symptoms.
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A New, Highly Mutated COVID Variant Called 'Cicada' Is Spreading in the US. Know These Symptoms
The heavily mutated new BA.3.2 COVID-19 variant, aka "cicada," is circulating in at least 25 U.S. states, the CDC said. What to know about its spread and symptoms.
Caroline Kee
Updated March 27, 2026

BA.3.2, a heavily mutated new COVID-19 variant which may be better able to escape immunity from vaccines or prior infection, is now spreading in the United States.

Although COVID cases are currently low nationally, the BA.3.2 strain is gaining traction around the globe. BA.3.2, aka "cicada," emerged over a year ago and slowly simmered until last fall, when it started ramping up in several countries, including the U.S.

As of Feb. 11, BA.3.2 has been detected in at least 25 states, the U.S. Centers for Disease Control and Prevention said.

Perhaps more concerning is the variant's slew of genetic changes in its spike protein, which set it apart from other variants circulating, Andrew Pekosz, Ph.D., a virologist at the Johns Hopkins Bloomberg School of Public Health, tells TODAY.com.

The SARS-CoV-2 virus mutates constantly as it spreads, which leads to the emergence of new variants. Most of the strains spreading right now are closely related, with slight genetic differences. But BA.3.2 stands out, according to experts.

“It has a lot of mutations that may cause it to look different to your immune system,” Pekosz says.

These have the potential to reduce protection from a previous infection or vaccination, according to a new study published in the CDC's latest Morbidity and Mortality Weekly Report.

As a result, the “hyper-mutated” strain is being closely tracked by public health officials. In December 2025, the World Health Organization classified BA.3.2 as a “variant under monitoring."

BA.3.2 was nicknamed “cicada” by T. Ryan Gregory, Ph.D., a professor of evolutionary biology at the University of Guelph who's coined other variant names like “stratus” and “pirola.”

Like its namesake insect, BA.3.2 also spent its first few years “underground” before re-emerging as a potential major variant, Gregory tells TODAY.com.

Here's what to know about BA.3.2, where it's spreading, symptoms and the effectiveness of current vaccines.

What Is the New COVID Variant, BA.3.2?

BA.3.2 was first identified in November 2024 in South Africa. It's a descendent of BA.3, an omicron subvariant that emerged in 2022 and briefly circulated with BA.1 and BA.2, the CDC said.

Its ancestor BA.3 fizzled out, but never disappeared, says Pekosz. Two years and dozens of mutations later, BA.3.2 emerged. It further branched into two subvariants, BA.3.2.1 and BA.3.2.2.

Since 2024, BA.3.2 has moved slowly and quietly, overshadowed by dominant variants like Nimbus and XFG — which all descend from BA.2. Last September, BA.3.2 started taking off.

"It was under the radar, replicating, until it started to spread more from person to person," says Pekosz.

BA.3.2 has 70–75 mutations in its spike protein — that’s a lot, says Pekosz — which set it apart from JN.1 and LP.8.1, the strains targeted by current COVID-19 vaccines.

According to the CDC, BA.3.2 represents a new lineage that's “genetically distinct” from the family of variants we’ve seen in recent years. “We think it might be able to evade a lot of the immunity already in the population,” says Pekosz.

In laboratory studies, BA.3.2 effectively escaped COVID-19 antibodies due to its spike protein changes, the CDC said.

"What's interesting, however, is some of these mutations may actually make the virus bind less well to our cells. So yes, our immune system may not recognize it, but it also doesn't recognize us as well," Dr. Dana Mazo, an infectious diseases physician at NYU Langone Health, tells TODAY.com.

Why is BA.3.2 resurfacing now? That’s unclear, Mazo says.

Does the New COVID Variant Cause More Severe Illness?

Is BA.3.2 making people sicker? Fortunately, no.

"There’s no evidence that BA.3.2 is causing more severe disease or hospitalizations in countries where it’s more widespread," Dr. Adolfo García-Sastre, director of the global health and emerging pathogens institute at Mt. Sinai, tells TODAY.com.

"It can still cause problems, of course, but it's not a more problematic strain that previous ones," says García-Sastre.

Pekosz adds: “It looks scary on paper, but it hasn’t really made a big impact in terms of disease in most places yet.”

Where Is BA.3.2 Spreading?

As of Feb. 11, 2026, BA.3.2 has spread to at least 23 countries, per data from the CDC and the Global Initiative on Sharing All Influenza Data (GISAID) database. It's driving about 30% of cases in Denmark, Germany and the Netherlands, per the CDC.

BA.3.2 was first detected in the U.S. in June 2025 in a traveler returning from the Netherlands at the San Francisco International Airport, the CDC said. Since then, it's been detected in international travelers, COVID patients and wastewater samples.

BA.3.2 is spreading in at least 25 states, per the CDC:
  • California
  • Connecticut
  • Florida
  • Hawaii
  • Idaho
  • Louisiana
  • Maine
  • Maryland
  • Massachusetts
  • Michigan
  • Missouri
  • Nevada
  • New Hampshire
  • New Jersey
  • New York
  • Ohio
  • Pennsylvania
  • Rhode Island
  • South Carolina
  • Texas
  • Utah
  • Vermont
  • Virginia
  • Wyoming

Currently, BA.3.2 is not fueling enough cases to be included in the CDC’s variant proportion tracker.

However, according to the latest wastewater monitoring data from the CDC, the BA.3.2 variant was found in least 11% of samples, nationally, during the week ending Mar. 21.

Data from WastewaterSCAN, a Stanford University-run program that tracks diseases, also show increasing detections of BA.3.2 in sewage samples across the country.

“There are still a lot of unknown questions about how prevalent it is in the U.S., because surveillance has been reduced a lot,” García-Sastre says.

Will BA.3.2 Cause a Surge in the U.S.?

Although BA.3.2 detections are going up, it's still circulating at a relatively low level in many countries, including the U.S. "It's increasing, but it hasn't really caused a huge surge of infections anywhere," Pekosz adds.

Cicada hasn't overtaken the current dominant variants, XFG (stratus), NB.1.8.1 (nimbus) and their descendants, Gregory adds.

Despite the large mutations in its spike protein, "BA.3.2 has not shown a sustained growth advantage over other any other co-circulating variant," the WHO said.

"If it had really special advantages, we'd probably have seen it take off and dominate globally relatively quickly. We didn't see that, but it's not going away, so it's something to keep an eye on," says Pekosz.

Even if BA.3.2 can evade existing immunity, there will likely still be some “cross-reactivity," so it won't be a complete stranger to our immune systems, the experts say.

COVID-19 can be unpredictable, so only time will tell. “It may evolve to be bit better at spreading or causing disease, but we just don’t know,” says Pekosz.

However, it's unlikely that BA.3.2 will cause a wave as large or severe as the ones seen very early in the pandemic, he adds.

Symptoms of the New COVID Variant BA.3.2

The symptoms of BA.3.2 are similar to those caused by other variants circulating right now, the experts note.

According to the CDC, common COVID-19 symptoms in 2026 include:
  • Cough
  • Fever or chills
  • Sore throat
  • Congestion
  • Shortness of breath
  • Loss of smell or taste
  • Fatigue
  • Headache
  • Gastrointestinal symptoms

Symptoms can vary depending on the person, but usually go away on their own with supportive care.

"The new variant is still sensitive to COVID antiviral drugs that we have been developing, so at least those will work," says García-Sastre.

Do Vaccines Protect Against the New COVID Variant?

BA.3.2 has drawn attention partly because the changes in its spike protein have may affect how well the vaccine protects against infection, highlighting the need for possible reformulation, the experts note.

The 2025-2026 COVID vaccines, which target the JN.1 lineage, are effective at protecting against severe disease from current strains.

In lab studies, these vaccines were less effective against BA.3.2, but more research is needed, the CDC said.

"It's not completely clear how effective the current vaccine will be, but it likely still has some effectiveness," García-Sastre says.

According to the WHO, current COVID vaccines "are expected to continue providing protection against severe disease."

Vaccines are typically reformulated in the summer and can protect against multiple strains. "One beauty of this vaccine is that we can update it every year," says Mazo.

In the meantime, you can still protect yourself and others by testing if you have symptoms, staying home when sick and wearing a mask in high-risk (crowded, indoor) settings.

If you haven't been vaccinated or infected with COVID in the last six to 12 months, it may be worth talking to your doctor about whether a booster is right for you, says García-Sastre.

Vaccination is particularly important for people at higher risk of severe disease from COVID-19, which include adults over 65 and individuals with weakened immune systems or underlying conditions.

"Vaccination is still going to help limit cases," says Pekosz.
 
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THE END OF ACIP? DR. ROBERT MALONE SAYS AN HHS INSIDER IS WORKING AGAINST LEADERSHIP - The HighWire

mRNA vaccine pioneer Robert Malone, MD examines reports that the Advisory Committee on Immunization Practices (ACIP) may be disbanded—a development that could signal a major shift in U.S. vaccine policy. As a key advisory body to the Centers for Disease Control and Prevention (CDC), ACIP has...
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DEL BIGTREE INTERVIEW OF ROBERT MALONE - VIDEO AT LINK 41 MIN 46 SEC

THE END OF ACIP? DR. ROBERT MALONE SAYS AN HHS INSIDER IS WORKING AGAINST LEADERSHIP
MARCH 26, 2026

mRNA vaccine pioneer Robert Malone, MD examines reports that the Advisory Committee on Immunization Practices (ACIP) may be disbanded—a development that could signal a major shift in U.S. vaccine policy. As a key advisory body to the Centers for Disease Control and Prevention (CDC), ACIP has long shaped national immunization schedules and guided which vaccines are recommended across the country.

Dr. Malone explains how ACIP’s influence extends far beyond recommendations, impacting insurance coverage, school requirements, and federal vaccine programs. Its potential removal raises critical questions about how future vaccine decisions will be made, who will assume that authority, and what standards will guide public health policy moving forward.

In a striking development, Dr. Malone also raises concerns about internal dynamics within the Department of Health and Human Services (HHS), alleging that a “mole” inside the agency may be undermining the Secretary’s agenda. The claim adds a new layer of tension to an already evolving landscape, highlighting concerns about transparency, internal alignment, and accountability within federal health institutions.

As scrutiny of public health agencies intensifies, these reported changes are being viewed by some as a push for reform, while others see potential disruption to long-standing systems. Looking ahead, Dr. Malone explores what this could mean for vaccine development, authorization pathways, and informed consent.

If ACIP’s role is diminished or eliminated, it may fundamentally reshape how vaccines are evaluated and recommended in the United States—marking a potential turning point in the future of public health policy.
 
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Persistent SARS-CoV-2 Fragments Linked to Long COVID
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 20, 2026


Medical News: Study Explores Why Symptoms May Last Long After Infection
A new scientific review is shedding light on a key question that has puzzled doctors and patients alike: why do some people continue to feel unwell long after recovering from COVID-19?

Researchers now suggest that remnants of the SARS-CoV-2 virus may remain in the body for extended periods, potentially contributing to ongoing symptoms known as long COVID.

The study was conducted by scientists from the Functional Food Research Institute at the Industry-University Cooperation Foundation, the Department of Foodcare YAKSUN, and the Department of Food Science and Biotechnology, all based at Daegu Haany University in Gyeongsan-si, Republic of Korea.


Viral Remnants Found in Multiple Organs
According to the review, traces of the virus—including RNA and proteins—have been detected in various organs even after the acute infection phase has ended. These include the lungs, heart, brain, gastrointestinal tract, and kidneys.

In the lungs, viral material may persist within immune cells that are unable to fully clear it. In the heart, remnants have been associated with inflammation that could affect cardiovascular function. In the brain, viral signals have been linked to neurological symptoms such as memory issues and difficulty concentrating.

The gastrointestinal tract appears to be a particularly important site. Because it contains high levels of receptors that the virus uses to enter cells, viral fragments may remain there long after respiratory symptoms subside.


How Viral Fragments Remain in the Body
Unlike viruses that become dormant, SARS-CoV-2 does not appear to establish a classic latent infection. Instead, it may leave behind fragments that the immune system cannot completely eliminate.

These fragments can persist in immune cells such as macrophages, which engulf viral particles but may retain them instead of fully destroying them. The virus also has the ability to interfere with normal immune responses, reducing the body’s ability to detect and clear infected cells. In some individuals, especially those with underlying health conditions or weakened immunity, this may increase the likelihood of persistent viral material.


Link to Long COVID Symptoms
This Medical News report highlights that these lingering viral components may continuously stimulate the immune system, even in the absence of active infection.

As a result, the body may remain in a state of low-grade inflammation. This ongoing immune activity is believed to contribute to many long COVID symptoms, including fatigue, shortness of breath, muscle pain, and cognitive difficulties.

In addition, the persistence of viral proteins—particularly the spike protein& mdash;may trigger abnormal immune responses. In some cases, this could lead to autoimmune-like reactions where the body mistakenly attacks its own tissues.


Evidence From Clinical and Laboratory Studies
The findings are supported by multiple studies that have detected viral RNA and proteins in tissue samples, body fluids, and immune cells.

Advanced techniques such as PCR testing and imaging methods have confirmed the presence of viral material in different parts of the body months after infection.

However, researchers emphasize that detecting viral fragments does not necessarily mean the virus is still active or capable of spreading. In most cases, these are likely non-infectious remnants.

Still, the possibility of low-level viral activity in certain tissues cannot be completely ruled out.


Implications for Treatment
The presence of persistent viral material has important implications for how long COVID is managed.

Researchers are exploring whether antiviral medications could help eliminate remaining viral fragments. Drugs used during acute COVID-19, including protease inhibitors and monoclonal antibodies, are being studied for potential benefits in long COVID patients.

At the same time, treatments aimed at regulating the immune system are also under investigation. These include anti-inflammatory medications and targeted therapies designed to reduce chronic immune activation.

Currently, most treatment approaches focus on relieving symptoms rather than addressing the underlying cause.


Conclusion
The growing evidence that SARS-CoV-2 fragments may persist in the body provides an important piece of the long COVID puzzle, but it does not yet offer definitive answers. While studies clearly show that viral RNA and proteins can remain in multiple organs, the exact role these remnants play in causing ongoing symptoms is still being investigated.

What is becoming increasingly clear is that these lingering viral components may contribute to sustained immune activation and chronic inflammation in some individuals. Further research is essential to determine whether targeting these remnants can lead to effective treatments and improved recovery for those affected by long COVID.

The study findings were published in the peer reviewed journal: COVID.
 
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Study Reveals That an Impaired Innate Immune System is Likely Behind Long COVID Manifestations
Study Reveals That an Impaired Innate Immune System is Likely Behind Long COVID Manifestations
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 20, 2026


Medical News: Understanding Why Symptoms Linger After COVID-19
A new scientific review is shedding light on one of the biggest medical mysteries of the pandemic—why millions of people continue to suffer from Long COVID long after the initial infection has passed. Researchers now believe that the root cause may not be the virus itself lingering in the body, but rather a failure of the body’s innate immune system to properly switch off after fighting the infection.

The study was conducted by scientists from the Department of Microbiology and Molecular Genetics, University of the Punjab, Lahore, Pakistan; the School of Veterinary Medicine and Biomedical Sciences, University of Nebraska–Lincoln, USA; and the Department of Biology, University of Ottawa, Canada.


The Immune System That Won’t Turn Off
Normally, when the body fights an infection, the immune system activates inflammation to kill the virus and then shuts down once the threat is gone. However, in Long COVID patients, this shutdown process appears to be broken. Instead of calming down, the immune system continues to stay active. This creates a cycle of ongoing inflammation that can damage tissues and lead to symptoms such as fatigue, brain fog, breathlessness, and heart issues.

Researchers describe this as a failure of “immune resolution”—a process that is supposed to restore the body back to normal after illness. In Long COVID, this reset mechanism simply does not work properly.


Hidden Triggers Keep the Fire Burning
One key discovery is that leftover fragments of the virus may remain in the body, especially in areas like the gut, lungs, or nasal passages. These remnants do not cause infection but continue to irritate the immune system.

At the same time, other hidden triggers may worsen the problem. These include reactivation of dormant viruses like Epstein-Barr virus, and leakage of bacterial toxins from the gut due to a weakened intestinal barrier.

Together, these factors continuously stimulate immune sensors, keeping the body in a constant state of alert.


Damage Signals Add Fuel to the Problem
The study also found that damaged cells release alarm signals that further activate the immune system. These signals, known as danger molecules, create a feedback loop where inflammation leads to more damage, and more damage leads to even more inflammation.

This ongoing cycle explains why symptoms can persist for months or even years in some individuals.


The Body’s Repair System Is Also Failing
Another critical issue is that the body’s natural repair system is not functioning properly. Normally, special molecules help stop inflammation and promote healing. However, in Long COVID patients, these molecules are either reduced or ineffective.

In addition, immune cells that are supposed to clean up dead cells are not working as they should. This leads to a buildup of cellular debris, which further worsens inflammation.

This Medical News report highlights that the immune system is essentially stuck in “fight mode,” unable to transition into recovery.


Long-Term Changes in the Immune System
Perhaps most concerning is that the infection may permanently alter immune cells. The study found that immune cells can undergo long-lasting changes in how they behave, making them either overly aggressive or unusually weak.
These changes can persist long after the virus is gone, helping explain why Long COVID is so difficult to treat.


Conclusion
The findings strongly suggest that Long COVID is not simply a lingering infection but a complex immune disorder where the body fails to properly shut down inflammation and repair itself. This ongoing immune dysfunction, driven by persistent triggers and faulty recovery mechanisms, creates a self-sustaining cycle of symptoms. Understanding this process opens the door for new treatments aimed at restoring immune balance rather than just targeting the virus itself.

The study findings were published in the peer reviewed journal: Clinical Immunology.
 
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Herbal Breakthrough Slows Deadly Lung Inflammation
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 22, 2026

A team of researchers from the College of Chinese Materia Medica, Chongqing University of Chinese Medicine, the College of Traditional Chinese Medicine, Chongqing Medical University, and the Institute of Pharmacology and Toxicology, Chongqing Academy of Chinese Materia Medica have uncovered promising evidence that a traditional herbal remedy may help control life-threatening lung inflammation linked to sepsis and viral infections.

This Medical News report highlights how the plant Eupatorium lindleyanum DC. could play a crucial role in calming the dangerous immune overreaction known as a “cytokine storm,” a condition often seen in severe infections including COVID-19.


What Makes Cytokine Storms So Dangerous
When the body fights infection, it releases proteins called cytokines to help coordinate the immune response. However, in severe cases, this process goes into overdrive, flooding the body with excessive inflammatory signals. This “cytokine storm” can damage organs, especially the lungs, leading to breathing failure and even death.

The researchers focused on this problem because both sepsis and viral infections like COVID-19 share this same harmful mechanism. Finding a treatment that can safely calm this response could save many lives.


The Herbal Candidate Under Study
Eupatorium lindleyanum DC., a plant long used in traditional Chinese medicine, is known for its anti-inflammatory and antiviral properties. However, until now, scientists had not fully understood how it works inside the body.

The research team used a combination of laboratory experiments, animal studies, and computer simulations to explore its effects in detail. They identified 32 active compounds within the plant, many of which interact with key biological pathways linked to inflammation.


Key Findings from the Study
The results were striking. In animal models with severe lung injury, the herbal extract significantly reduced swelling, bleeding, and immune cell buildup in lung tissue. According to findings shown in lung tissue analysis, treated subjects had visibly healthier lung structures compared to untreated ones.

The herb also lowered levels of major inflammatory molecules such as TNF-a and IL-6—two of the main drivers of cytokine storms. Importantly, these reductions were dose-dependent, meaning higher doses led to stronger effects.

In cell-based experiments, the extract successfully blocked inflammatory signaling pathways, particularly NF-?B and PI3K–Akt. These pathways are known to act like “on switches” for inflammation. By turning them down, the herb effectively reduced excessive immune activity.


A Powerful Compound Called Hyperoside
One standout compound identified in the pl ant is hyperoside. The study showed that it binds strongly to key proteins involved in inflammation and viral infection, including ACE2—the receptor used by SARS-CoV-2 to enter cells.

In further experiments, hyperoside reduced lung damage in mice exposed to a coronavirus-like pseudovirus. It also lowered ACE2 levels and suppressed genes linked to inflammation, suggesting both anti-inflammatory and antiviral potential.


Why This Discovery Matters
These findings suggest that Eupatorium lindleyanum DC. works through multiple pathways at once. Instead of targeting just one part of the disease process, it acts broadly—reducing inflammation, protecting lung tissue, and potentially interfering with viral activity.


Conclusion
The study provides strong evidence that this traditional herbal medicine could offer a new approach to treating severe lung inflammation caused by infections. By targeting multiple biological pathways simultaneously, it may help control cytokine storms more effectively than single-target drugs. While further clinical studies in humans are needed, the results are highly encouraging and point toward a future where natural compounds could complement modern treatments in managing life-threatening inflammatory conditions.

The study findings were published in the peer reviewed journal: Current Issues in Molecular Biology.
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Back in the '80s I had bronchitis (got it every year in October/November and held on to it until May, when the weather warmed up.

Went to the local health food store and asked what was good for my condition.

The employee took me to a bottle of herbs called Chinese Lung Herbs. It was a bit pricey, but I was desperate.

It knocked the bronchitis right out of me.

Forward to the early 2000s and I went back to get another bottle. Couldn't find it. Asked an employee and she didn't have a clue what I was talking about.

Guess the FDA didn't like how well it worked. Couldn't find it on a Web search either. Very disappointed. Not surprised.

I take Vitamin D3, K-2, Magnesium Glycinate and Zinc on an almost daily basis (I've missed a couple of days this week) and haven't had bronchitis in almost three decades.
 
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Autoantibodies implicated as drivers of long COVID in new study
by University Medical Center Utrecht
edited by Stephanie Baum, reviewed by Robert Egan
March 24, 2026

A growing body of evidence suggests that long COVID (or post-COVID syndrome), a condition affecting more than 10% of people after a SARS-CoV-2 infection, may be driven by the immune system turning against the body. Now, new research coordinated by UMC Utrecht and Amsterdam UMC provides some of the strongest functional evidence yet that autoantibodies (antibodies that mistakenly target the body's own tissues) could play a causal role. The work appears in Cell Reports Medicine.

Long COVID is known for its wide range of symptoms, including extreme fatigue, post-exertional malaise (PEM), pain, and cognitive dysfunction ("brain fog"). Despite its prevalence, the biological mechanisms behind the condition remain poorly understood. Previous studies have hinted at immune dysregulation and the presence of autoantibodies, but whether these molecules actively drive symptoms has remained unclear.

Antibodies that transfer symptoms

In the study, researchers injected immunoglobulin G (IgG, a major class of antibodies), derived from the blood of 34 patients with long COVID, into mice. The result was striking, as the animals developed persistent pain-like hypersensitivity. This effect lasted for at least two weeks. Even more notable, IgG collected from the same patients two years later reproduced the same symptoms when administered to mice.

Co-study lead Prof. Niels Eijkelkamp, Ph.D. (Center for Translational Immunology, UMC Utrecht) explains, "This finding suggests that the underlying disease mechanism may persist long after the initial infection, potentially explaining why many patients experience long-term symptoms."
Distinct biological subgroups

To better understand the condition, researchers analyzed blood samples from long COVID patients and identified distinct subgroups based on markers of brain injury (GFAP, NFL) and immune activation (interferon-ß). These subgroups displayed unique molecular signatures in large-scale protein analyses.

When autoantibodies from these different groups were tested in mice, they produced distinct patterns of symptoms. Co-study lead Jeroen den Dunnen, Ph.D. (Center for Infection and Molecular Medicine, Amsterdam UMC) added, "This finding supports the idea that long COVID is not a single condition but a heterogeneous disease with different biological drivers."

A landscape of autoimmunity

The team also found that long COVID patients carry elevated levels of autoantibodies that target a wide range of the body's own proteins, from those involved in immune regulation, nerve signaling, and metabolism. Many of these autoantibodies persisted for years and differed between the specific patient subgroups.

"What is really striking," say both co-leads of the study, "is that three independent research groups have recently reported similar findings, adding confidence to the emerging autoimmune signature of long COVID." In addition, in other diseases with overlapping symptoms, patient-derived antibodies can also induce symptoms in animal models, such as fibromyalgia, pointing to shared immunological pathways.

Toward targeted treatments

While the study has limitations, including its relatively small size, single-center design and the use of pooled samples, it provides compelling evidence that IgG autoantibodies may actively contribute to long COVID symptoms. The results also point toward new treatment strategies. Therapies that are able to remove or neutralize harmful antibodies, such as immunoadsorption, plasmapheresis or targeted immunotherapy, could offer relief, particularly if tailored to specific biological subtypes.

As researchers continue to unravel the complexity of long COVID, this study marks an important step toward understanding and potentially treating this persistent and often debilitating condition.

Publication details
H.J. Chen et al, Transfer of IgG from Long COVID patients induces symptomology in mice, Cell Reports Medicine (2026). DOI: 10.1016/j.xcrm.2026.102693. www.cell.com/cell-reports-medi … 2666-3791(26)00110-2
Journal information: Cell Reports Medicine
Provided by University Medical Center Utrecht
 
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Magnetic Therapy Shows Promise for Long COVID Brain Fog
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 25, 2026

A new clinical study is offering fresh hope to millions struggling with lingering brain fog after COVID-19, suggesting that a simple at-home magnetic therapy device could significantly improve memory, attention, and mood.

Researchers from the Department of Rehabilitation and Human Performance and the Department of Medicine at the Icahn School of Medicine at Mount Sinai, along with collaborators from Fareon, Inc, conducted a randomized controlled trial exploring a novel treatment called Microtesla Magnetic Therapy (MMT). Their findings point toward a safe, non-invasive approach that may tackle one of the most frustrating symptoms of long COVID—cognitive impairment.


Understanding Long COVID Brain Fog
Long COVID affects a significant portion of people even months after infection, with symptoms ranging from fatigue to memory problems. Cognitive impairment, often described as “brain fog,” can disrupt daily life, making it difficult to concentrate, process information, or recall simple details.

Scientists believe this condition is linked to ongoing inflammation in the brain, damage to blood vessels, and dysfunction in mitochondria, the energy-producing structures within cells. These issues create a cycle of reduced energy and persistent inflammation that affects brain performance.


How Magnetic Therapy Works
MMT is a wearable device that delivers very low-level radiofrequency magnetic fields to the brain. Unlike traditional brain stimulation therapies, it does not directly stimulate nerve cells but instead targets inflammation and cellular stress.
Participants in the study used the device at home for 15-minute sessions twice a week over four weeks. The therapy was designed to be simple, with remote monitoring ensuring correct usage.

In this Medical News report, the key innovation lies in the therapy’s ability to potentially reduce inflammation and oxidative stress in the brain—two major drivers of cognitive decline in long COVID patients.


Strong Improvements in Memory and Focus
The study involved 30 participants with moderate-to-severe cognitive symptoms linked to long COVID. They were divided into two groups: one receiving active therapy and the other a sham treatment.

By the eight-week mark, those using the active device showed statistically significant improvements in several cognitive tests. These included better working memory, improved verbal recall, and faster processing speed. For example, memory recall scores improved noticeably compared to the control group, and attention-related tasks also showed measurable gains.

Beyond the statistically significant outcomes, many other cognitive measures—including attention span, executive function, and processing speed—showed encouraging trends, suggesting broader benefits that may beco me clearer in larger studies.


Mood and Quality of Life Also Improve
Interestingly, the therapy did not just affect cognition. Participants reported better emotional well-being and reduced fatigue. Standardized assessments showed significant improvements in emotional health scores and a meaningful reduction in tiredness.

Depression and anxiety symptoms also improved, although these changes were not always statistically significant when compared to the control group. Still, the overall pattern indicates that the therapy may support both mental clarity and emotional stability.


Safe, Easy, and Highly Practical
One of the most striking findings was the safety and usability of the treatment. Participants completed 100 percent of their therapy sessions, and no device-related adverse effects were reported.

Users found the device comfortable and easy to operate, highlighting its potential for widespread home use. This is especially important for long COVID patients who may struggle with energy levels and mobility.


What This Means Moving Forward
While the study was relatively small, its findings are highly promising. The improvements in cognition and mood, combined with the absence of side effects, suggest that MMT could become a valuable tool in managing long COVID symptoms.

However, researchers caution that larger trials are needed to confirm these results and better understand how the therapy works at a biological level.


Conclusion
This study highlights a potentially game-changing approach to treating long COVID brain fog. By targeting inflammation and cellular dysfunction rather than simply masking symptoms, Microtesla Magnetic Therapy offers a new direction in recovery. Its ease of use, safety, and early signs of effectiveness make it particularly appealing for long-term management. If future studies confirm these findings, this technology could significantly improve quality of life for millions still struggling with the cognitive aftermath of COVID-19.

The study findings were published on a preprint server and are currently being peer reviewed.
www.medrxiv.org

Microtesla Magnetic Therapy for cognitive impairment in post-acute sequelae of SARS CoV-2: A randomized controlled feasibility study

Background Cognitive impairment has significant implications for function and quality of life and is common in individuals with post-acute sequelae of SARS CoV-2, also known as long COVID (LC). Emerging evidence suggests that sustained neuroinflammation, cerebrovascular dysfunction, and...
www.medrxiv.org www.medrxiv.org
 
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Multi-Strain Probiotics Show Promise in Long COVID Recovery
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 26, 2026

Probiotics are emerging as a potential supportive therapy for individuals suffering from long COVID, according to a new study examining how gut bacteria influence recovery after infection. Researchers found that a multi-strain probiotic formulation can modestly improve gut microbial balance and may help reduce inflammation linked to persistent symptoms.


The Gut Link in Long COVID
Long COVID is characterized by ongoing symptoms such as fatigue, cognitive issues, and digestive disturbances that persist months after the initial infection. Increasing evidence suggests that disruptions in the gut microbiome play a role in prolonging these symptoms. An imbalance in gut bacteria can contribute to chronic low-grade inflammation and metabolic dysfunction, both of which are commonly seen in long COVID patients.


Study Design and Participants
The study covered in this Medical News report, was conducted by researchers from the Innovation Centre of the Faculty of Technology and Metallurgy, University of Belgrade; the Department of Gastroenterology and Hepatology at the Clinic for Internal Medicine, University Hospital Medical Center “Bežanijska Kosa”; the Faculty of Medicine, University of Belgrade; and the Department of Biochemical Engineering and Biotechnology, Faculty of Technology and Metallurgy, University of Belgrade, Serbia.

A total of 74 participants were analyzed, including individuals with long COVID, recovered patients, and healthy controls. Participants in the intervention group received a multi-strain probiotic for 12 weeks, while others served as controls.


Probiotic Composition
The multi-strain probiotic contained Saccharomyces boulardii, Lacticaseibacillus rhamnosus GG, and two strains of Lactiplantibacillus plantarum. These strains are known for their roles in supporting gut integrity, regulating immune responses, and influencing metabolic activity.


Key Microbiome Findings
The probiotic did not significantly alter overall gut microbial diversity. However, it led to selective changes in specific bacterial groups. In individuals with long COVID, beneficial bacteria associated with metabolic balance and immune regulation increased. These included genera linked to anti-inflammatory effects and improved gut function.

At the same time, certain bacteria associated with inflammatory states showed a reduction or failed to increase, suggesting a shift toward a more balanced microbial environment. These effects were more pronounced in long COVID participants compared to recovered individuals.


Functional Changes in Gut Activity
Beyond compositional changes, the probiotic also influenced the functional activity of gut microbes. There was an increase in pathways related to energy metabolism and redox balance, indicatin g improved microbial efficiency and cellular processes. These changes are relevant because long COVID has been associated with impaired metabolic function.


Effects on Inflammation and Biochemical Markers
The study also evaluated blood-based health markers. Participants receiving probiotics showed consistent trends toward reduced inflammation, including lower levels of C-reactive protein. Improvements in liver-related enzymes were also observed, indicating a potential systemic benefit beyond the gut.

Although these changes were modest and did not always reach statistical significance, the overall pattern suggested a beneficial effect on inflammatory and metabolic processes.


Implications for Treatment
The findings suggest that probiotics may play a supportive role in managing long COVID by targeting gut microbiota. Rather than causing major shifts, probiotics appear to fine-tune microbial composition and function, which may help restore balance in individuals with disrupted gut ecosystems.


Conclusion
Multi-strain probiotic supplementation was associated with targeted improvements in gut microbiota composition and function, particularly in individuals with long COVID. The observed increases in beneficial bacteria, along with trends toward reduced inflammation and improved metabolic markers, indicate that probiotics may contribute to recovery by supporting gut and systemic health. While the effects are moderate, they are consistent and biologically meaningful. Larger randomized studies are needed to confirm these findings and to determine optimal formulations and treatment durations.

The study findings were published in the peer reviewed journal: Microorganisms
 
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Peptides from the Diatom Microalgae Phaeodactylum Tricornutum Exhibit Antiviral Properties Against SARS-CoV-2
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 26, 2026

Scientists are continuing to search for safer and more effective ways to fight COVID-19, especially as new variants keep emerging. A new study has now revealed that a marine microalgae called Phaeodactylum tricornutum could provide a natural solution. Researchers found that tiny protein fragments, known as peptides, derived from this microalgae show strong antiviral activity against SARS-CoV-2 while remaining safe for human cells.


A Natural Source of Antiviral Compounds
Marine microalgae are increasingly being studied because they produce a wide range of bioactive compounds. These natural substances are often less toxic and more compatible with the human body compared to synthetic drugs. In this case, scientists focused on peptides obtained from Phaeodactylum tricornutum, a fast-growing microalgae known for its rich protein content and ability to produce useful biological molecules.


Who Conducted the Study
The research was carried out by scientists from the Laboratorio de Virología Molecular at the Unidad de Investigación Biomédica de Zacatecas, Instituto Mexicano del Seguro Social; the Facultad de Medicina at Universidad Autónoma de Sinaloa; the Department of Infectomics and Molecular Pathogenesis at CINVESTAV-IPN; the Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”; Investigadores por México (SECIHTI); and the Faculty of Medicine at Autonomous University of Sinaloa, all based in Mexico.


How the Study Was Done
Researchers extracted proteins from the microalgae and broke them down into smaller peptides. These peptides were grouped based on their size and then tested on human lung cells infected with the SARS-CoV-2 Omicron variant. The goal was to evaluate both their safety and their ability to reduce viral infection.


Strong Safety Profile Observed
One of the most important findings was the low toxicity of these peptides. Even at high concentrations, most of the peptide groups did not significantly damage the human cells. Larger peptide groups, particularly those in the 10–30 kDa and 5–10 kDa range, maintained high levels of cell survival.

In contrast, a commonly studied antiviral drug used for comparison showed a clear increase in toxicity as its concentration increased. This suggests that the microalgae-derived peptides may offer a much safer alternative.


Powerful Antiviral Effects
The study also showed that these peptides can effectively reduce SARS-CoV-2 infection in cells. Smaller peptides worked quickly at lower doses but produced inconsistent results. Larger peptides, however, showed stronger and more reliable antiviral effects as their concentration increased.

At higher doses, the larger peptide groups were able to reduce infection levels to nearly the same as uninfected cells. This indicates that they may interfere with the vir us’s ability to replicate or infect new cells.


Why Size Makes a Difference
An important discovery was that the effectiveness of these peptides depends on their size. Larger peptides appear to interact more strongly with key viral components, making them more stable and effective at blocking infection.

This Medical News report highlights that while smaller peptides may act faster, larger peptides provide more consistent and sustained antiviral activity, making them more suitable for future drug development.


Better Balance Between Safety and Effectiveness
Compared to the reference antiviral drug used in the study, the microalgae peptides demonstrated a better balance between safety and antiviral activity. They were able to reduce viral infection while maintaining high cell viability, which is a key factor in developing safe treatments.


What Comes Next
Researchers plan to identify the specific peptides responsible for the antiviral effects and understand how they work at a molecular level. Further studies in more advanced biological models and eventually in humans will be needed before these findings can be translated into real-world treatments.


Conclusion
This study offers promising evidence that marine microalgae could become an important source of new antiviral therapies. The peptides derived from Phaeodactylum tricornutum showed strong ability to reduce SARS-CoV-2 infection while maintaining a high safety profile in laboratory conditions. Their size-dependent effectiveness provides valuable insight into how natural compounds can be optimized for better results. With continued research, these peptides could play a key role in developing safer and more effective antiviral treatments for COVID-19 and other emerging viral threats.

The study findings were published in the peer reviewed journal: Marine Drugs.
 
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Increase in NT-proBNP Levels After COVID-19 mRNA Vaccines Raises New Questions
Nikhil Prasad Fact checked by:Thailand Medical News Team
Mar 29, 2026

A new scientific investigation has uncovered subtle but noteworthy changes in heart-related biomarkers following mRNA COVID-19 vaccination, even among healthy individuals. While the findings do not point to immediate danger, they are prompting deeper questions about how the body responds to these widely used vaccines at a microscopic level.


Understanding What Researchers Looked For
Scientists focused on specific blood markers that signal heart stress or damage. These included NT-proBNP, a substance released when the heart is under strain, and cardiac troponins, which typically rise when there is actual heart injury.

The study involved 83 healthy adult volunteers, primarily military personnel aged between 18 and 55, who received two doses of mRNA COVID-19 vaccines. Blood samples were collected multiple times before and after vaccination, allowing researchers to track even small biological changes over time.

The research team came from several respected institutions, including the Third Faculty of Medicine, Charles University; the Institute for Clinical and Experimental Medicine in Prague; Thomayer University Hospital; Bulovka University Hospital; Czech Technical University in Prague; and the Institute of Aviation Medicine.


A Temporary Spike in Heart Stress Marker
One of the most striking findings was a temporary increase in NT-proBNP levels, especially within the first two weeks after the second vaccine dose. On average, levels rose significantly compared to pre-vaccination measurements.

Nearly half of the participants experienced a rise of at least 1.5 times their normal baseline levels shortly after the second shot. Despite this, none of the participants reached levels typically associated with heart failure or serious cardiac conditions.

Importantly, these elevated levels did not persist. Within a few weeks, NT-proBNP values returned to normal, suggesting that the effect was short-lived.


No Evidence of Heart Damage
While NT-proBNP increased, the study found no corresponding rise in troponin levels, which are considered a more direct indicator of heart muscle injury. This distinction is critical.

In simple terms, the heart may have been under temporary stress, but there was no sign of actual damage.

Researchers also noted that none of the participants developed symptoms such as chest pain, shortness of breath, or swelling, which would indicate clinical heart problems.


Why Does This Happen
The researchers believe the explanation may lie in the body’s immune response. Vaccines are designed to trigger inflammation as part of building immunity. This immune activation can influence the cardiovascular system in subtle ways.
The study observed that inflammatory markers also increased briefly after vaccination, suggesting that the immune response might indirectly place temporary stress on the heart.

This hailandmedical.news/">Medical News report highlights that such biological responses are not entirely unexpected and may occur even in the absence of disease.


Who Was Most Affected
Although the findings were not statistically strong enough to confirm clear risk factors, certain trends emerged. Higher NT-proBNP increases were seen more often in men, individuals without prior COVID-19 infection, and those without underlying health conditions.

There were also slight indications that the Moderna vaccine might be associated with higher increases compared to Pfizer-BioNTech, though the sample size was too small for firm conclusions.


What This Means Going Forward
The findings raise new questions about the COVID-19 mRNA vaccines. The study adds an important layer of understanding. It shows that even in healthy people, the body undergoes measurable cardiovascular changes after vaccination, albeit temporary and without clinical consequences.


Conclusion
This study provides valuable insight into how the human body reacts to mRNA COVID-19 vaccines at a deeper physiological level. The temporary rise in NT-proBNP suggests that the heart may experience short-lived stress following vaccination, particularly after the second dose. However, the absence of troponin elevation and clinical symptoms strongly indicates that this response does not translate into actual heart damage. These findings highlight the importance of continued monitoring and research, especially in populations with existing cardiovascular conditions or higher risk profiles.

The study findings were published in the peer reviewed journal: Vaccine.
 
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