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[Heliobas Disciple]

Lay summary on plausibility of more extended O-glycosylation as a last resort for SARS-CoV-2 immune escape

For those who find it too challenging to read my most recent findings on the impending evolution of the SARS-CoV-2 virus...

voiceforscienceandsolidarity.substack.com

(fair use applies)

EMPHASIS FROM ORIGINAL (not mine)


Lay summary on plausibility of more extended O-glycosylation as a last resort for SARS-CoV-2 immune escape
Geert Vanden Bossche
Jan 19, 2026

For those who find it too challenging to read my most recent findings on the impending evolution of the SARS-CoV-2 virus (From Enhanced Infectiousness to Enhanced Virulence: Why a Glycosylation-Driven Shift in SARS-CoV-2 Evolution Has Become Increasingly Likely), here follows a four-page lay summary:

Lay Summary - What This Manuscript Says About the Future of COVID-19

Most people assume that viruses naturally become milder over time - that as our immune systems adapt, the virus evolves to cause less serious disease and eventually becomes a harmless, endemic virus like one that causes the common cold.

This manuscript argues that this widely held belief may not apply to the ongoing evolutionary dynamics of SARS-CoV-2 (SC-2)- the virus that causes COVID-19 (C-19) - because the immune environment created by widespread C-19 vaccination and repeated vaccine-breakthrough infections is unlike anything we’ve seen before. Under these unique conditions, the virus may neither die out nor simply become milder. Instead, it may be driven by evolution toward very different traits, including a sudden shift that could make it very dangerous (‘highly virulent’) in highly C-19-vaccinated populations.


1. How immune pressure shapes viral evolution

When a virus enters a community, the immune defense of that community/ population pushes back. This ‘immune pressure’ comes from:

• Antibodies [Abs] (from vaccination or previous infections)
• T cells that kill virus-infected cells
• Innate immune responses triggered early in infection

If immune pressure is low (as in a mostly unexposed population), the virus can spread easily and may gradually adapt to low-resistance conditions. If immune pressure is very high and sterilizing (completely blocking infection), it can stop the virus from spreading at all.

But in many places, especially highly C-19-vaccinated countries, adaptive immune responses are very strong -for example, in form of high titers of Spike (S)-specific Abs-yet still insufficient to fully block the virus. This leads to vaccine-breakthrough infections (VBTIs), as exemplified by Omicron, where non-neutralizing Abs protect against severe disease while still allowing:

• Mild infections
• Continued transmission
• Repeated exposures over time

This situation creates a unique evolutionary environment that generates repeated VBTIs. On a backdrop of high anti-S Ab titers, which typically occur in highly C-19-vaccinated populations, these VBTIs refocus the immune response onto less immunogenic S regions, yielding weaker neutralizing Ab responses-and thus, perpetuating a cycle of suboptimal immune pressure and viral immune escape due to failure of the population’s immunity to stop viral transmission (i.e., due to lack of ‘herd immunity’!).


2. Early evolution focused on transmissibility and antibody escape

Over the first years of the pandemic, SC-2 evolved mainly by:

• Becoming more infectious
• Evolving mutations in the S protein that help it evade some Abs

Omicron and its descendants became dominant, or co-dominant, because they partially escaped population-level immune responses targeting the S protein while increasing intrinsic infectiousness; they could, therefore, spread more easily in populations highly vaccinated with S-based C-19 vaccines. But these changes have limits. There is only so much the S protein can change before it stops working properly.


3. What happens when simple mutations run out of room?

The S protein can tolerate many mutations, but:

• Too many changes can destabilize the protein
• Some mutations reduce the virus’s ability to enter cells
• The virus can hit structural limits

As the virus accumulates changes to escape immunity, it eventually reaches a point where additional small mutations no longer improve its ability to survive and spread.

At that point, the virus may need a new evolutionary strategy - something different from simply tweaking the S protein’s amino acids.


4. Glycosylation: a different way to adapt

Proteins like the coronavirus S are naturally coated with sugars - a process called glycosylation. These sugar molecules are added by human cells as the viral proteins are being made.

Glycosylation can:

• Hide parts of the virus from Abs
• Change how the virus interacts with cells
• Influence how the immune system ‘sees’ the virus

The manuscript proposes that as the virus becomes more constrained in how much it can change its protein structure, it may instead evolve by changing how its S protein is glycosylated - that is, how the sugars are attached.

This type of change doesn’t involve altering the virus’s genetic sequence in the same way as a mutation does, but it can still change the virus’s behavior in important ways.


5. Antigen (Ag) presentation and immune system bypass

One of the most important ideas in this manuscript is that changes in glycosylation may allow the virus to bypass a critical part of the immune system called antigen (Ag) presentation.

Normally:

1. Infected cells show bits of the virus on their surface, thereby enabling ‘Ag presentation’.
2. T cells recognize these bits and kill the infected cell.
3. This limits the spread of the virus inside the body.

But if glycosylation changes how the virus interacts with the immune system, those infected cells may not show the virus effectively to T cells. In other words, the virus can spread without triggering the strongest antiviral responses.

This is not just hiding from Abs - it is bypassing the cornerstone of the immune alert system.


6. How the virus could spread differently

In addition to bypassing Ag presentation, glycosylation changes might shift the way the virus enters new host cells.

Instead of:

• Attaching to ACE2 receptors on susceptible cells
• Entering and replicating directly

The virus may:

• Bind to receptors on immune cells such as dendritic cells patrolling the upper respiratory tract
• Hitch a ride, so to speak, on these cells
• Infect other host cells and further propagate through direct cell-to-cell transfer

This process - called trans-infection and trans-fusion - allows the virus to spread while avoiding immune defenses that would normally detect and kill virus-infected cells.


7. What this means for disease severity

These shifts could lead to:

• Faster and wider spread of the virus inside the entire body
• Less immune recognition
• Higher likelihood of overwhelming viral replication

In populations that are heavily C-19 vaccinated, where traditional immune responses are already shaping how the virus evolves, this could lead to:

• Hyperacute cases of virulent VBTIs
• Higher rates of systemic virus dissemination
• A huge and sudden surge of illness and death

It is reasonable to assume that the population segment generating the immune conditions that served as a breeding ground for numerous post-Omicron immune escape variants will also be most affected by SC-2’s adaptation into a potentially highly virulent coronavirus (so-called HI-VI-CRON).

Hence, enhanced virulence does not reflect the virus ‘wanting’ to be more harmful but rather the remaining evolutionary options under strong, incomplete immune pressure from the vaccine-primed part of the population.


8. Why unvaccinated people would be less affected

Ironically, the manuscript suggests that people who are unvaccinated and have not built up strong S-targeted immunity may not drive this kind of viral evolution. Because their immune systems do not exert adaptive pressure on the virus, healthy unvaccinated individuals have not driven its evolution toward drastic immune escape strategies. Consequently, healthy unvaccinated people are highly unlikely to serve as a breeding ground for HI-VI-CRON.


9. Why this could happen in many places at once

Because the evolutionary pressure comes from the shared immune environment in highly C-19-vaccinated populations - not from a single location or “patient zero” - similar glycosylation-driven shifts could happen independently in different countries at about the same time.

That means:

• The virus does not need to spread from one place to another to change.
• It can undergo similar changes in any highly C-19-vaccinated population as these populations are characterized by strong but incomplete collective immunity.

10. Viral evolution does not imply viral attenuation

This manuscript does not predict a specific timeline - it doesn’t say ‘this will happen next week or next month.’ But it does argue that:

• The traditional view of viruses always becoming milder over time is not based on any scientific rationale.
• Under intense but incomplete population-level immune pressure, the virus may be pushed into a sudden and dramatic evolutionary shift.
• One possible result of that shift is an increase in virulence in certain populations.

In conclusion: Evolution doesn’t aim for mildness - it aims for survival. Under strong, mismatched immune pressure, survival can look very different from what most people expect. Indeed, at this stage of the pandemic, almost nobody expects SC-2 to become highly virulent. That’s why it cannot be overemphasized that society in highly C-19-vaccinated regions risks being caught off-guard!

The manuscript encourages scientists, clinicians, and the public to broaden how we think about viral evolution and to pay attention to the immune pressures we create as we implement irrational public-health strategies and administer non-sterilizing vaccines to entire populations in the midst of an acute viral pandemic.


Take-home message

The absence of worsening clinical signals during the emergence of newly circulating variants does not imply intrinsic attenuation of SC-2 or its transition toward endemicity but instead sets the stage for the selection of additional, virulence-enabling O-glycosylation as last-resort mechanism of viral immune escape.

Dismissing alternative evolutionary trajectories for SC-2 because they are uncomfortable or unprecedented does not reflect scientific consensus but results from historical extrapolation erroneously applied to a host-pathogen system that has fundamentally broken all historical assumptions as a direct consequence of the mass C-19 vaccination program.



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For those more scientifically minded, he also did a 4 page scientific summary (vs. the lay summay above) which goes into more detail which can be found here:

Scientific Summary (4 pp.) on 'Plausibility of more extended O-glycosylation as a last resort for SARS-CoV-2 immune escape'

For those who find it too time-consuming to read my most recent findings on the impending evolution of the SARS-CoV-2 virus...

voiceforscienceandsolidarity.substack.com

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/sars-cov-2-new-variants-found-to-boost-endocytic-entry-while-keeping-fusion-intact

(fair use applies)


SARS-CoV-2 New Variants Found to Boost Endocytic Entry While Keeping Fusion Intact
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 14, 2026


Medical News: Omicron’s New Trick Revealed
In a discovery that adds a surprising twist to the ongoing evolution of SARS-CoV-2, German scientists from the University Hospital Regensburg, the University of Regensburg, and the Leibniz Institute for Immunotherapy have shown that newer Omicron subvariants are getting better at using an alternative doorway to enter human cells. The research team analyzed nine real patient isolates collected from 2020 to 2022, tracing how the virus has gradually shifted toward more efficient endocytic entry while still holding on to its original TMPRSS2-driven fusion pathway. Their findings provide fresh insights into why Omicron spreads so easily yet often causes milder symptoms in healthy individuals.

This Medical News report highlights how this dual-entry ability may offer the virus a powerful evolutionary advantage—especially in the upper airways where Omicron thrives.


How the Virus Gets Inside Cells
SARS-CoV-2 can enter human cells in two major ways.

-Direct membrane fusion relies on the enzyme TMPRSS2. This pathway was heavily used by early variants like Alpha and Delta.

-Endocytosis, however, is a slower but more flexible route that depends on cathepsin enzymes inside the cell.

Using four human cell lines including Calu-3, Caco-2, A549hACE2+/TMPRSS2+ and HEK293T, the researchers tested how each variant responded to two inhibitors:

• Camostat, which blocks TMPRSS2-mediated fusion

• Aloxistatin, which blocks cathepsin-driven endocytosis

Detailed findings charts show that earlier variants were mostly stopped by camostat, proving strong reliance on TMPRSS2. Omicron strains, however—especially BE.1.1 and BA.5.1—were much more sensitive to aloxistatin, revealing a clear shift toward endocytic uptake.


Mutations That Shift the Balance
The study identified key spike-protein mutations common to the endocytosis-favoring strains:
• D69/D70 deletion
• L452R substitution
• F486V substitution

According to the study findings, these precise changes co-occur in BE.1.1 and BA.5.1—the two strains that replicated well in endocytosis-dominant HEK293T cells.

The researchers also found evidence that a mutation in the M protein, D3N, which is typical of BA.4/BA.5 lineages, may further enhance endocytic entry.


What This Means for Public Health
The study suggests SARS-CoV-2 has not abandoned its original entry route. Instead, it has expanded its toolkit. Omicron still uses TMPRSS2-dependent fusion, meaning it can still infect lower-lung cells—an ongoing risk for the elderly and immunocompromised. But its enhanced endocytic entry likely boosts replication in the upper airways, driving higher transmissibility.


Conclusion
The findings reveal that SARS-CoV-2 continues to evolve in ways that optimize both spread and survival. By preserving its fusion-based entry while strengthening endocytic uptake, Omicron has broadened its cell tropism and enhanced its ability to infect a wider range of tissues. This dual strategy helps explain why the virus remains highly transmissible, adaptable and persistent. Continued monitoring is essential, especially as new variants build upon this expanding entry toolkit and potentially reshape future infection patterns.

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

Frontiers | SARS-CoV-2 evolution enhances endocytic uptake while preserving TMPRSS2-dependent fusion

BackgroundOf the five SARS-CoV-2 variants-of-concern (VOC), Omicron shows increased transmissibility and infectivity, but lower pathogenicity. This drop in v...

www.frontiersin.org

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/study-finds-that-nearly-everyone-exposed-to-covid-19-developed-persistent-lung-impairment

(fair use applies)


Study Finds That Nearly Everyone Exposed to COVID-19 Developed Persistent Lung Impairment!
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 16, 2026


Medical News: A New Wave of Post-Virus Illness
In what experts are calling a “silent second pandemic,” new research from Romania reveals that almost all individuals infected with COVID-19 continue to struggle with lingering lung problems months—even years—after recovering from the initial illness. Many are not even be aware that they are suffering from pulmonary impairments!

This alarming discovery shows that irrespective of whether patients had mild or moderate COVID-19, many show measurable lung impairment long after the virus has left the body, adding weight to fears that Long COVID is reshaping healthcare demands.


Thousands Living with “Invisible” Breathlessness
The study followed 97 adults confirmed with post-COVID-19 syndrome, meaning they still had symptoms at least three months after infection. Researchers tracked breathlessness, coughing, exhaustion and the ability of the lungs to move oxygen into the bloodstream. Even up to 22 months after infection, many patients—especially those who had moderate disease—showed abnormal test results.

Small and large lung capacities were assessed through standardized lung function testing. While oxygen saturation readings often appeared normal, deeper tests revealed the lungs were struggling.


Lung Function Falls—Then Recovers Slowly
A clear pattern emerged:
-Lung volume (FVC) drops for months after infection
-Recovery happens slowly and unevenly over 9–18 months
-But the lungs rarely return fully to normal

Individuals who had moderate COVID-19 fared much worse. Their breathing capacity (FVC), airflow strength (FEV1) and gas exchange ability (DLCO and KCO) were all markedly lower than in those with mild infections.

Most importantly, gas transfer—the lung’s ability to push oxygen into the bloodstream—remained impaired in many patients past the one-year mark. This suggests long-lasting injury deep in the lung tissue.


The “Damage Signature” Left Behind
Advanced statistical analysis confirmed three types of lung damage shaping the lives of COVID-19 survivors:

-Obstructive issues affecting small airways

-Restrictive lung loss, reducing total breathing capacity

-Diffusion impairment, limiting oxygen entry into blood

These were found both early after infection and more than a year later, meaning millions worldwide could unknowingly have altered lung structure from the virus.

This Medical News report underscores that the effects extend beyond breathlessness. Many participants reported exhaustion, difficu lty exercising and coughing—symptoms doctors warn are easy to dismiss.


Who Is Most at Risk?
Certain groups were hit hardest:

-Adults over 50

-People with hypertension, diabetes or obesity

-Anyone who experienced moderate or severe COVID-19

Even patients with no known lung disease before infection suffered measurable impairment.


A Clear Warning for the Future
The researchers say their findings signal a long-term challenge. COVID-19 doesn’t simply disappear when the fever breaks—it leaves behind a legacy of injury. They caution that hospitals should brace for increased lung disease, rehabilitation needs and chronic respiratory care.


Conclusion
Taken together, the study paints a sobering picture: recovery from COVID-19 is much slower and more incomplete than originally believed. Even people who appeared to recover well may continue living with hidden lung damage, reduced oxygen exchange and weakened breathing capacity. The findings demonstrate the need for long-term follow-up, targeted rehabilitation, and greater investment in managing Long COVID, as millions may require support years after infection.

The study findings were published in the peer reviewed Journal of Clinical Medicine.

https://www.mdpi.com/2077-0383/15/2/717

 

[Heliobas Disciple]

A Pandemic Panic for Two Mutations, but None for Fifty!

Based on (increasingly scarce!) global genomic surveillance data, the current SARS-CoV-2 (SC-2) variant landscape-as inferred from available sequencing-appears to be dominated by several co-circulating lineages.

voiceforscienceandsolidarity.substack.com

(fair use applies)


A Pandemic Panic for Two Mutations, but None for Fifty!
Geert Vanden Bossche
Jan 22, 2026

Based on (increasingly scarce!) global genomic surveillance data, the current SARS-CoV-2 (SC-2) variant landscape-as inferred from available sequencing-appears to be dominated by several co-circulating lineages. These include XFG, NB.1.8.1 and LP.8.1 (all Omicron-derived lineages undergoing continued incremental mutation), BA.2.86 and its descendants (notably JN.1 with multiple sublineages), as well as BA.3.2 (nicknamed ‘Cicada’) and its derived sublineages, including RE.1.1 and RE.2.2.

The BA.3.2-derived lineages display a particularly noteworthy evolutionary behavior. Across multiple regions-including Australia, several European countries, and parts of the United States-they show a slow but steady increase in prevalence. Although Cicada sublineages may exhibit a modest growth advantage over some co-circulating lineages such as XFG or NB.1.8.1, they are not yet clearly dominant and do not (yet?) outcompete other major lineages at the global level.

BA.3.2-derived variants carry more than 50 spike (S) protein mutations relative to ancestral BA.3 and over 70 mutations relative to the original Wuhan strain. These changes are distributed across both the receptor-binding domain (S-RBD) and the N-terminal domain (S-NTD) of S. Notably, additional mutations in these domains are now accumulating convergently across multiple evolving lineages, frequently affecting determinants of ACE2-mediated viral entry and antibody-mediated immune recognition. This pattern is consistent with continued viral evolution under sustained immune pressure rather than simple directional selection for intrinsic transmissibility.

The observed evolutionary behavior of BA.3.2-derived sublineages is indeed difficult to reconcile with a model of simple directional selection for either increased intrinsic transmissibility or increased intrinsic virulence. Despite carrying an unusually large and diverse constellation of S mutations, including extensive remodeling of both the S-NTD and the S-RBD, these lineages have expanded only slowly, display no clear or sustained growth advantage over competing variants (see above), and have not been associated with marked changes in clinical severity.

Within a classical evolutionary framework, such extensive mutational remodeling would be expected either to confer a decisive fitness advantage or to result in rapid lineage extinction. The persistence of substantial mutational diversity that fails to translate into clear fitness superiority must therefore be interpreted, in evolutionary terms, as a hallmark of constraint rather than optimization. In other words, the maintenance of BA.3.2-derived lineages within a relatively narrow prevalence range suggests that they are evolving under strong constraints, consistent with mounting immune pressure acting not on individual epitopes, but on a higher-order phenotypic trait, namely viral transmissibility.

This implies that further gains in intrinsic viral transmissibility through incremental amino-acid substitutions are becoming increasingly sterically and functionally constrained. The absence of a sharp growth advantage despite extensive S remodeling is thus more consistent with immune-constrained replication than with benign attenuation or adaptive optimization.

Moreover, the lack of major clinical shifts despite pronounced antigenic change supports the interpretation that the virus is being forced to trade intrinsic fitness for immune evasion, rather than progressing toward reduced pathogenicity. In this context, slow propagation combined with increasing mutational convergence should be viewed as a diagnostic signal of near-threshold immune pressure on viral transmission, rather than as evidence of evolutionary stasis or endemic stabilization.

Such a high mutational effort yielding only marginal phenotypic gain is entirely consistent with a system approaching an evolutionary bottleneck imposed by population-level immune pressure on viral transmissibility. Under these conditions, further adaptation through conventional amino-acid remodeling becomes progressively ineffective, as previously described (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape). This evolutionary regime would instead favor selection of a qualitatively different escape strategy-for example, a glycosylation-driven phase transition that decouples viral spread from classical antigen presentation and immune-mediated clearance, rather than continued incremental mutation.

In conclusion, the convergence of additional mutations within the S-NTD and S-RBD across circulating variants, together with the slow expansion, limited growth advantage, and clinical neutrality of newly emerging, heavily mutated BA.3.2-derived sublineages, is incompatible with a model of unconstrained directional selection for increased intrinsic transmissibility or virulence. Rather, this evolutionary pattern strongly indicates viral adaptation under escalating immune pressure acting on the phenotype of transmissibility, not benign attenuation.

Taken together, these observations suggest that SC-2 is approaching a constrained evolutionary state in which qualitative, rather than incremental, adaptive shifts become selectively favored. As previously argued (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape), it is therefore scientifically reasonable to postulate that such a phase transition could precipitate the emergence of high virulence in highly C-19–vaccinated populations.

In light of this concern, a striking asymmetry has emerged in the global perception of viral risk. A handful of amino-acid substitutions in a seasonal or avian influenza virus, often detected in a limited number of isolated cases with little or no sustained human-to-human transmission, are sufficient to trigger urgent headlines, emergency briefings, and speculative modeling of a potential influenza pandemic. Entire policy discussions are launched on the basis of what might happen if such changes were to accumulate.

By contrast, the ongoing evolution of SC-2-characterized by dozens of mutations across the S protein, extensive antigenic remodeling, recurrent recombination, and clear signatures of convergent evolution under population-level immune pressure-largely passes without alarm. Viral variants carrying far greater molecular novelty than those that provoke influenza panic are routinely dismissed as ‘benign,’ ‘stable,’ or ‘endemic-adapted,’ often solely because they have not yet produced an immediately obvious clinical catastrophe.

Indeed, this naïve complacency appears to stem from the observation that the accumulation of large numbers of S mutations (often exceeding 50 relative to BA.3) has not been accompanied by major clinical changes previously associated with certain Omicron descendants (e.g., BA.2.86 or XBB-derived lineages). However, the absence of an immediate phenotypic signal does not imply evolutionary irrelevance, particularly in a virus evolving under unprecedented immune pressure within highly C-19-vaccinated host populations.

The discrepancy blows me away. Influenza is feared for what it could become on the basis of a few hypothetical mutations, whereas SC-2 is ignored, or normalized, despite all the mutations it’s actively incorporating in real time.

One virus is treated as an existential threat based on theoretical risk; the other as a solved problem despite displaying evolutionary dynamics without historical precedent. This is not balanced risk assessment. It is selective, willful blindness.

 

[Heliobas Disciple]

Lay summary on recent Substack article: "A Pandemic Panic for Two Mutations, but None for Fifty!"

For those who find it too challenging to read my recent Substack article (“A Pandemic Panic for Two Mutations, but None for Fifty!”), here follows a two-page lay summary:

voiceforscienceandsolidarity.substack.com

(fair use applies)


Lay summary on recent Substack article: "A Pandemic Panic for Two Mutations, but None for Fifty!"
Geert Vanden Bossche
Jan 23, 2026

For those who find it too challenging to read my recent Substack article (“A Pandemic Panic for Two Mutations, but None for Fifty!”), here follows a two-page lay summary:

Here’s something that genuinely baffles me.

When scientists detect one or two mutations in a seasonal or avian flu virus, often in just a handful of people and with no sustained spread, alarm bells go off. Headlines scream ‘potential pandemic!’ Emergency meetings are held. Models are built around what might happen if those mutations ever pile up.

But at the same time, SARS-CoV-2 (SC-2) is quietly evolving right in front of us, accumulating dozens of mutations, reshaping its spike (S) protein, recombining, and showing clear signs that it is adapting under strong immune pressure- and almost nobody seems worried.

Let’s look at what’s actually happening.


What the virus is doing right now

Global sequencing (what little of it remains) shows several SC-2 lineages circulating at the same time. Among them is a group derived from a variant called BA.3.2, nicknamed ‘Cicada.’

These Cicada variants are not exploding in cases. They’re not grabbing headlines. Instead, they’re doing something more subtle, and more interesting:

- They are slowly but steadily spreading in places like Australia, parts of Europe, and the US

- They carry more than 50 S mutations compared to earlier Omicron variants

- They have over 70 mutations compared to the original Wuhan virus

- Many of these mutations affect how the virus enters cells and how the immune system recognizes it.

Despite all these changes, they’re not causing obvious new waves of severe disease.


Why that matters

In normal viral evolution, you’d expect one of two things:

· Either all those mutations give the virus a big competitive advantage, and it takes over fast

· Or they weaken the virus, and the lineage dies out

But that’s not what we’re seeing! Instead, these heavily mutated variants are persisting without taking over. That’s a classic sign of constraint, not success. It suggests the virus is running into limits-trying many changes but getting very little payoff.

In simple terms:
The virus is working very hard for very little gain. It behaves like a virus running out of evolutionary room. That usually means it’s being pushed, not drifting naturally.


What’s pushing it?

The pressure doesn’t seem to be about a single mutation or antibody target. It looks broader. The virus appears to be under population-level immune pressure on transmission itself, more particularly in highly C-19-vaccinated populations.

That kind of pressure doesn’t select for viruses that improve their fitness in the usual evolutionary way, such as spreading faster or outcompeting other variants. On the contrary, it corners it as it narrows the evolutionary options. Many paths are blocked. Only a few narrow routes remain. And when that happens, biology often doesn’t respond with small tweaks but rather with major qualitative shifts.


Why this isn’t “benign evolution”

Because despite all these mutations:

• There’s no clear growth advantage
• No clear attenuation
• No clear stabilization of the viral evolutionary dynamics

Instead, we see:

• Slow spread
• Repeated convergence on similar mutations
• Lots of genetic effort for minimal benefit

That’s not what a virus looks like when it’s peacefully settling into endemic life!

It’s what a system looks like when it’s approaching a bottleneck!

Instead of making the virus ‘better’ at spreading in the usual way, the mounting population-level immune pressure on its transmissibility may push it to change how its surface is coated with sugars (a process called glycosylation). These sugar coatings can act like camouflage, helping the virus evade immunity and spread through alternative pathways in the body. While this may help the virus survive immune pressure exerted by highly C-19-vaccinated populations, this kind of escape doesn’t lead to a milder virus but carries a real risk of increased virulence.


The double standard

And here’s the part that really blows me away.

• Influenza is feared for what it might become with a few mutations
• SC-2 is dismissed despite what it is already doing-right now, at global scale

One virus triggers panic based on theory. The other is ignored, or at most ‘normalized’ despite unprecedented real-world evolution. That’s not reasonable risk assessment. That’s selective blindness. Once again, those who follow this shortsighted narrative risk being caught off guard.

 

[Heliobas Disciple]

150 Million Chinese People Have Pulmonary Nodules, State Outlet Reports

Authorities attribute the surge to more frequent scanning and promote insurance; Chinese citizens and an expert suspect there are other factors causing it.

www.theepochtimes.com

(fair use applies)


150 Million Chinese People Have Pulmonary Nodules, State Media Reports
Authorities attribute the surge to more frequent scanning and promote insurance; Chinese citizens and an expert suspect there are other factors causing it.
Alex Wu
1/17/2026

There are 150 million Chinese who have pulmonary nodules, as state media recently revealed.

The number of pulmonary nodules patients has increased rapidly in mainland China since the COVID-19 pandemic. The Chinese communist regime has attributed the increase to more frequent scanning. Chinese citizens and an expert have expressed skepticism towards the official rhetoric, suspecting there are more reasons behind the huge number of infections.

State-owned media outlet National Business Daily reported on Jan. 8 that the number of Chinese people with lung nodules detected through routine physical examinations has reached approximately 120 million to 150 million—a figure even exceeding the number of diabetes patients in the country.

The report also pointed out that lung cancer ranks first in both incidence and mortality among malignant tumors in China, with approximately 75 percent of patients being diagnosed at an advanced stage, citing data from the International Agency for Research on Cancer, an agency under the World Health Organization.

However, the report didn’t mention what caused the staggering number of pulmonary nodules patients in China.

China’s pulmonologist and the regime’s top respiratory infectious diseases advisor Zhong Nanshan told state media in 2025 that a major reason for the increasing number of people with pulmonary nodules is the significant increase in the number of people receiving CT scans after the COVID-19 pandemic, which has led to the discovery of more pulmonary nodules cases. Zhong said that there are many causes of pulmonary nodules, “in addition to the COVID-19, environmental pollution can also lead to their appearance.”

Zhong told the public not to panic about it, adding that “most pulmonary nodules are benign, but nearly 11 percent of them have malignant tendencies.”


Possible Reasons, Reasonable Doubts

This is not a sudden phenomenon, but the result of the accumulation of multiple factors, said Xiaoxu Sean Lin, associate professor of Biomedical Science, Fei Tian College Northern Campus in New York.

In addition to long-term exposure to environmental pollution, “long COVID (referring to symptoms lasting more than four weeks after COVID-19 infection) and problems related to Chinese domestic COVID-19 vaccines are the issues the authorities are most reluctant to address,” Lin told The Epoch Times.

COVID-19 has never left China, and many people have experienced repeated infections over the past few years, Lin said.

“The incidence of long COVID is very high, and the proportion of these patients with pulmonary nodules is also very high. Many people may still have pulmonary nodules even if they feel they have recovered from COVID-19.”

He pointed out that the early strains of coronavirus SARS-CoV-2 that caused COVID-19 “were most likely to cause lower respiratory tract infections,” noting that “when the virus first emerged in Wuhan, it primarily affected the lower respiratory tract, so lung infections were very common.”

In this situation, if the vaccine manufacturing process is substandard, “it will inevitably cause harm to some people, including developing pulmonary nodules,” Lin said.

The Chinese regime has never publicly disclosed the full extent of domestically produced COVID-19 vaccines’ side effects and long-term consequences.

“This is something the authorities are deliberately concealing,” Lin said. “Because the government doesn’t investigate, it’s very difficult for the public to see the full picture of the consequences of these COVID-19 vaccines.”

Mr. Liang, a patient with pulmonary nodules from Hebei Province who didn’t give his full name for safety concerns, told The Epoch Times that he developed pulmonary nodules after receiving the Sinovac COVID-19 vaccine in January 2021.

“I also developed several autoimmune diseases, including severe allergic asthma, chronic pharyngitis, mitral and tricuspid valve regurgitation, and Hashimoto’s thyroiditis, all of which appeared after receiving the vaccine,” he said.

“Almost everyone I know who received the vaccine has pulmonary nodules.”

After two years of seeking redress in vain, he said he and other people who suffer the same situation believe that “the medical association and the CDC experts are all in cahoots; it’s almost impossible for them to admit that it’s a side effect of the vaccine.”

Qian Dalong, a citizen in Beijing and a rights activist who had a stroke after being injected with Chinese-made COVID-19 vaccine, told The Epoch Times that pulmonary nodules are “a common and insignificant condition compared to strokes, which are more prevalent after getting Chinese COVID-19 vaccines.”
“Those seeking redress for injuries from COVID-19 vaccines are the group facing the most severe suppression and persecution from the Chinese regime, with many being arrested,” he said, adding that both central and local authorities do everything to “evade compensation responsibility.”


Promoting State-Backed Insurance

National Business Daily dedicated most of the article to promoting insurance for pulmonary nodules.

It said that West China Hospital of Sichuan University, in collaboration with insurance and technology companies, launched the nation’s first “digital therapy for comprehensive management of pulmonary nodules” in the first half of 2025. They claim it can cover hundreds of millions of people with pulmonary nodules.

Lin pointed out that this type of “insurance for people with preexisting conditions,” while seemingly innovative, actually “to some extent shifts public dissatisfaction with the state’s healthcare issues” and “transforms skepticism about government health care deficits into a new form of commercial health insurance to fill the financial gap.”

 

[Heliobas Disciple]

Navy issues apology to service members discharged under Biden-era vaccine mandate

Under Secretary apologizes to service members removed under the Biden administration’s COVID vaccine mandate

nypost.com

(fair use applies)


Navy issues apology to service members discharged under Biden-era vaccine mandate
By Fox News
Published Jan. 24, 2026, 1:00 p.m. ET

The Department of the Navy issued an apology letter Friday to former military personnel “unjustly removed” from service because of the COVID vaccine mandate during the Biden administration.

Under Secretary of the Navy Hung Cao emphasized that the Department of War is committed to “righting past wrongs” and welcoming back former service members who were dismissed during the pandemic.

“To the sailors and marines who were wrongfully discharged during COVID, we failed you,” Hung said in a video posted on X. “We will never allow this to happen again, not on my watch. We are ready for you to come back, and we want to correct your records.”

Cao, the Department of the Navy’s chief operating and chief management officer, overseeing roughly one million Navy, Marine Corps and civilian personnel, acknowledged the impact of the mandate on those it forced out.

“We are righting this wrong and it starts with this formal letter of apology,” he said.

President Trump signed Executive Order 14184 shortly after returning to office last January, directing federal agencies to identify service members affected by the former vaccine requirement and take steps to reinstate them or restore certain benefits.

The order applies to former members of the Army, Air Force, Marine Corps, Navy, Space Force and Coast Guard who were discharged solely for refusing the COVID-19 vaccine.

The former secretary of defense mandated in 2021 that all service members receive the COVID-19 vaccine, a policy that was rescinded in 2023.

“The military unjustly discharged those who refused the vaccine, regardless of the years of service given to our Nation, after failing to grant many of them an exemption that they should have received,” Trump’s executive order states.

The Department of War issued guidance to all the secretaries of military departments to contact former service members with information about potential reinstatement and to correct their discharge records.

According to the Department of Veterans Affairs, more than 8,000 service members were separated after the Biden administration’s Department of Defense issued the vaccination mandate.

“It is unconscionable that thousands of former Service members who held true to their personal and religious convictions were not just separated, but separated with general (under honorable conditions), rather than honorable, discharge characterizations,” Secretary of War Pete Hegseth said in a December memo. “While many have applied for and received relief from our Military Department review boards, I believe the onus is on us to make this right.”

Hegseth said he directed a proactive review of personnel records to identify individuals involuntarily discharged solely for refusing the COVID-19 vaccine and facilitate appropriate discharge upgrades.

 

[Heliobas Disciple]

Scientists use AI to create a virus never seen before

Lab-grown life has taken a major leap forward as scientists use AI to create a new virus that has never been seen before.

www.dailymail.co.uk

(fair use applies)


Lab-grown LIFE takes a major step forward - as scientists use AI to create a virus never seen before
Wiliam Hunter
26 January 2026

Lab–grown life has taken a major leap forward as scientists use AI to create a new virus that has never been seen before.

The virus, dubbed Evo–F2147, was created by scientists from scratch using new technologies that could revolutionise the course of evolution.

With just 11 genes, compared to the 200,000 in the human genome, this virus is among the simplest forms of life.

However, scientists believe that the same tools could one day create entire living organisms or resurrect long–extinct species.

This artificial virus was specifically created to kill infectious and potentially deadly E. Coli bacteria.

Based on a wild virus known to infect bacteria, scientists used an AI tool called Evo2 to create 285 entirely new viruses from scratch.

While only 16 were able to attack the E. Coli, the most successful were 25 per cent quicker at killing bacteria than the wild variants.

However, previous research has raised concerns that AI–designed pathogens could themselves become a deadly threat to humanity.

This incredible breakthrough comes from the work of scientists at Genyro, a startup led by British scientists and entrepreneur Dr Adrian Woolfson.

Dr Woolfson told the Daily Mail: 'For the last 4 billion years, all life on Earth has evolved by the trial-and-error process of Darwinian evolution by natural selection, which lacks any foresight or intention.

'Natural evolution now has a co-author. That co-author, the emerging ability of AI-driven genome design and genome construction technologies, has the potential to exist alongside natural evolution.'

This has been made possible by the simultaneous development of two technologies: AI that can write genetic code, and new tools for assembling genes in the lab.

The AI tool Evo2 is much like the large language model chatbots ChatGPT and Grok, except that it has been trained on genetic codes rather than written text.

Evo2 was trained on nine trillion 'base pairs' – the individual As, Cs, Ts, and Gs that are the basic materials of DNA – to teach it how genes are put together.

This allows Evo2 to create entirely new codes for organisms that have never existed, specifically shaped to fit their designer's requirements.

At the same time, scientists have also created a new method for putting together artificial genomes, known as Sidewinder.

In the past, putting together an artificial genome was like trying to put the torn–up pages of a book together – it's possible, but only if you know what order they are supposed to be in.

Dr Kaihang Wang, inventor of the technology and assistant professor at the California Institute of Technology, compares Sidewinder to adding page numbers to these torn–up fragments.

Dr Wang told Pharmaphorum: 'In order to have a book, not only do we need to have the printed each individual page, you also need to arrange them into the correct order to form the book, right?

'And before us, DNA construction was kind of like in the era of you have the printing press, but you don't have the other thing called a page number to actually align and assemble the books in the right order.'

Thanks to this new technology, scientists can make long sequences of DNA in the lab with 100,000 times more accuracy.

That could make constructing artificial genomes 1,000 times cheaper and 1,000 times quicker.

With Sidewinder and Evo2, scientists now have the potential to create entirely new forms of life in just days, rather than weeks or months.

Right now, the virus Evo–F2147 is just about as complex as anything that scientists are able to create.

With just 5,386 base pairs of DNA code compared to the 3.2 billion found in humans, this virus is incredibly simple and isn't even considered living by some experts since it can't reproduce on its own.

However, this is an extremely exciting moment for researchers attempting to tackle the growing threat of antibiotic resistance.

Dr Samuel King and Dr Brian Hie, co–creators of the new virus, wrote in a blog post: Bacterial resistance to antibiotics represents one of the most pressing challenges in modern medicine, with resistant infections killing hundreds of thousands or more annually.

'We wanted to see if we could one day design phage therapies that could be resilient against bacterial evolution.'

In the future, the researchers hope that these technologies could be used to create antibacterial treatments or speed up the design and production of vaccines.

Dr Woolfson says: 'This has immediate utility in the production of so-called personalised cancer vaccines. These typically take eight to 12 weeks to manufacture, but with the Sidewinder technology that we have developed, we anticipate being able to do this in two to three days'

However, experts have previously suggested that the use of AI has the potential to speed up the production of bioweapons as well as medicines.

In a paper published last year, researchers used AI to design proteins that could mimic deadly poisons and toxins such as ricin, botulinum, and Shiga.

They found that a large number of these weaponizable DNA codes could slip past the safety filters used by companies that print custom DNA sequences on demand.

The researchers did this to demonstrate how our current biosafety tools might not be ready for the widespread availability of AI–designed life.

Likewise, experts on existential risk have warned that designing bioweapons is one of the most dangerous potential applications of AI.

The Existential Risk Observatory, which monitors threats to humanity's survival, considers an AI–designed plague to be one of the five biggest risks the world faces.

To avoid these new tools being used for dangerous means, the researchers behind Evo2 specifically removed examples from the training data that could teach the AI how to make human pathogens.

Dr King and Dr Hie write: 'Evo cannot generate human viral sequences due to deliberate training data exclusions, preventing both accidental and intentional misuse for pathogen design.'

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

How do you make a new virus in the lab?

• Scientists train an AI on trillions of pieces of genetic information.
• The AI, called Evo2, creates a sequence of DNA base pairs that gives the genetic code for a new virus.
• The scientists use a technology called Sidewinder to create small building blocks of DNA.
• Sidewinder attaches 'page number' labels to the building blocks so they can be put in the right order.
• The pieces are assembled into DNA, and the 'page numbers are removed'.
• The DNA is inserted into a bacterium, which is then hijacked to start producing the new virus.

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/gut-leak-tied-to-crushing-fatigue-in-long-covid

(fair use applies)


Gut Leak Tied to Crushing Fatigue in Long COVID
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 19, 2026

Long COVID continues to trouble millions worldwide, with sufferers reporting persistent exhaustion, brain fog, and problems controlling heart rate and blood pressure long after the initial infection has passed. Scientists are increasingly looking beyond the lungs and brain to understand why these symptoms linger. One emerging suspect is the gut, particularly a condition known as increased intestinal permeability, sometimes described as a “leaky gut.” This Medical News report explores new findings that shed light on this hidden connection.


Study Overview and Case Details
The study by medical researchers form Charité University Medicine Berlin-Germany focused on a 60-year-old woman who developed long COVID after a SARS-CoV-2 infection and endured severe fatigue and autonomic dysfunction for more than three years. Researchers repeatedly measured her intestinal permeability at five different time points using a carbohydrate absorption test, a method not previously reported in long COVID patients. This test compares how two sugars, lactulose and mannitol, pass through the gut lining into the urine.


Key Findings Explained Simply
Results showed that during periods when the patient’s fatigue and other symptoms worsened, her lactulose to mannitol ratio rose sharply, indicating a leakier gut barrier. When her symptoms eased, this ratio fell. A second COVID-19 infection caused another spike in intestinal permeability, again matching a flare in fatigue. Importantly, treatment with probiotics containing Bacillus coagulans and Bacillus subtilis, followed by a course of medicinal clay, was linked to measurable gut improvement and noticeable relief from fatigue.


Why These Findings Matter
This case strongly suggests that gut barrier damage may influence how severe long COVID symptoms become. It also hints that restoring gut health could help some patients feel better.


Conclusions
Overall, these findings support the idea that intestinal permeability may act as a biological marker and treatment target in long COVID, warranting larger studies to confirm cause, mechanism, and therapeutic potential.

The study findings were published as an abstract in the peer reviewed journal: Frontiers in Medicine.

Frontiers | Intestinal permeability correlated with chronic fatigue in a patient with long COVID – a case report and overview of the literature

Background: Long COVID is a complex condition characterized by persistent symptoms such as chronic fatigue, cognitive impairment, and autonomic dysfunction. ...

www.frontiersin.org

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/cinnamon-scents-show-promise-in-blocking-covid-19-infection

(fair use applies)


Cinnamon Scents Show Promise in Blocking COVID-19 Infection
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 19, 2026

A team of Japanese researchers has uncovered surprising evidence that common flavor and fragrance ingredients, especially those derived from cinnamon, may help reduce the risk of SARS-CoV-2 infection. The findings suggest that everyday food-related aromas could one day play a supportive role in limiting the spread of COVID-19, particularly through the mouth and upper respiratory tract.


Researchers And Institutions Behind the Study
The research was conducted by Japanese scientists from the Department of Microbiology and Immunology at Nihon University School of Dentistry at Matsudo, the Department of Bacteriology I at the National Institute of Infectious Diseases in Tokyo, and the Department of Orthodontics at Nihon University Dental School at Matsudo in Chiba, Japan. Their work focused on simple, affordable strategies that could complement existing prevention methods.


Why New Preventive Ideas Are Still Needed
Although vaccines and basic hygiene measures have greatly reduced severe illness, COVID-19 continues to spread due to new variants and silent transmission by people without symptoms. Many infections begin in the oral cavity, where the virus attaches to a protein called ACE2 found in saliva glands and mouth tissues. This Medical News report highlights how targeting this early stage of infection could be crucial in reducing transmission in daily life.


How Fragrances Were Tested Against the Virus
The scientists examined several well-known flavor and fragrance compounds to see if they could block the virus from infecting cells. In laboratory experiments, SARS-CoV-2 was mixed with different fragrance solutions and then added to cultured cells commonly used for virus research. The goal was to see whether these compounds could stop the virus from entering and damaging the cells.


Cinnamon Based Flavors Stand Out
Most of the tested fragrance compounds showed strong ability to reduce viral infection at certain concentrations. Among them, cinnamon flavor and cinnamon mint were especially effective, maintaining their protective effect even at lower doses compared to other compounds. Importantly, further testing confirmed that these fragrances did not harm the cells themselves, meaning the antiviral effect was not due to toxicity.


What Makes These Findings Important?
The researchers believe these fragrances may interfere with the physical process the virus uses to bind to human cells. Since the mouth is a major entry point for infection, foods or products containing such flavor compounds could potentially help lower the amount of virus in saliva and reduce spread, especially from people who do not yet feel sick.


Looking Toward Everyday Applications
The study also discusses how these findings could inspire new preventive habits. Products like candies, oral pastes, or specially designed foods might one day deliver sufficient amounts of these beneficial flavor compounds. However, more work is needed to improve how these substances dissolve and remain active in real-life products.


Conclusions
Overall, the research suggests that cinnamon flavor and cinnamon mint could become part of simple, low-cost strategies to help reduce SARS-CoV-2 transmission. While not a replacement for vaccines or masks, such approaches may add another layer of protection in daily life, especially as new variants continue to emerge and long-term effects of infection remain a concern.

The study findings were published in the peer reviewed journal: Current Research in Microbial Sciences.

https://www.sciencedirect.com/science/article/pii/S2666517424001184

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/covid-19-drug-calms-inflammation-but-risks-for-blood-vessel-damage-and-blood-clots-remain

(fair use applies)


COVID-19 Drug Calms Inflammation but Risks for Blood Vessel Damage and Blood Clots Remain
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 23, 2026

Severe COVID-19 has long been known to cause dangerous inflammation and abnormal blood clotting, increasing the risk of organ damage and death. A new clinical investigation now shows that while a commonly used immune drug can rapidly calm inflammation, problems in blood vessels and clot breakdown may continue longer than expected.

Researchers from Semmelweis University in Budapest, Szent György University Teaching Hospital of Fejér County, University of Szeged, Flór Ferenc County Hospital, University of Pécs, Szentágothai Research Centre, and Poznan University of Medical Sciences in Poland closely tracked how the blood systems of critically ill COVID-19 patients changed after treatment with tocilizumab, a drug that blocks the inflammatory molecule interleukin-6. This Medical News report highlights findings that may help doctors better understand lingering clotting risks in severe COVID-19 cases.


Why inflammation and clotting matter in COVID-19
In serious COVID-19 infections, the immune system can go into overdrive. High levels of inflammation damage the lining of blood vessels and trigger excessive clot formation. These clots can block blood flow in the lungs, heart, brain, and other organs. Tocilizumab is widely used to reduce this immune overreaction, but its effects on clotting and clot breakdown over time have remained unclear.


How the study was conducted
The study followed 15 critically ill COVID-19 patients in intensive care units across Hungary. All patients received tocilizumab and standard treatments such as steroids and blood thinners. Blood samples were taken before treatment and repeatedly over seven days. Researchers examined markers of inflammation, blood clot strength, vessel injury, and the body’s ability to dissolve clots.


Key findings explained simply
The results showed that inflammation dropped quickly after treatment. Levels of C-reactive protein, a key marker of inflammation, fell by more than 90 percent within days. Fibrinogen, a protein that makes blood clots thicker and stronger, also steadily declined.

However, markers linked to blood vessel injury, especially von Willebrand factor, continued to rise. This suggests that although inflammation improved, the blood vessel lining remained damaged. Tests of clot strength showed that clots stayed firm and resistant to breakdown, even as inflammation eased.

At the same time, signs of impaired clot dissolution persisted. Important clot-dissolving regulators increased in a way that slowed fibrinolysis, the natural process that breaks down clots. D-dimer levels, which reflect ongoing clot formation and breakdown, rose during the first days before slowly stabilizing.


What these results mean
Overall, the findings indicate that blo cking interleukin-6 helps control the inflammatory storm of COVID-19 but does not fully restore normal blood vessel function or clot behavior. The body appears to remain in a pro-thrombotic, or clot-prone, state for days after inflammation improves.


Conclusions
These findings show that severe COVID-19 is more than just an inflammation problem. Even when immune overactivity is successfully reduced, damage to blood vessels and resistance to clot breakdown can persist. This highlights the need for continued monitoring and possibly targeted therapies aimed at blood vessels and clotting systems, not just inflammation, to fully reduce complications and improve outcomes in critically ill patients.

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

https://www.mdpi.com/2227-9059/14/1/254

 

[Housecarl]

I've put this here instead of the WoW thread because this is more than a "weekly" subject......HC

Posted for fair use.......

Defending Against the Next Bioweapon: the mRNA Imperative

Modern synthetic biology and AI represent both medicine’s greatest breakthrough and warfare’s most terrifying evolution. In this new landscape, where

warontherocks.com

Cogs of War

Defending Against the Next Bioweapon: the mRNA Imperative​

Jeff Coller

January 28, 2026

Modern synthetic biology and AI represent both medicine’s greatest breakthrough and warfare’s most terrifying evolution. In this new landscape, where biological weapons can be designed faster than traditional defenses can be developed, recent government decisions risk abandoning our only countermeasure that can keep up: messenger ribonucleic acid, better known by its acronym, mRNA.

Known most famously for the prominent role it played in vaccinations against SARS-CoV-2 (the virus that causes COVID-19), mRNA is a medical platform that can generate new defenses in days rather than years. In layperson’s terms, mRNA amounts to a temporary set of instructions that tells cells how to make a specific protein.

It should be said upfront that as co-founder of Tevard Biosciences, a company developing tRNA-based (helper molecule that carries the right building blocks to the cell’s protein-making machinery) therapeutics for genetic diseases, I have a commercial stake in the broader RNA medicines field. I also co-founded the Alliance for mRNA Medicines, a nonprofit organization advancing mRNA technology. My perspective, however, is based on three decades of research in RNA biology — including work in my laboratory that contributed to the design of Spikevax, Moderna’s COVID-19 vaccine — and direct experience with the public-private coordination that made Operation Warp Speed possible.

To maintain this advantage, Congress should restore recently cut mRNA research funding, and the Pentagon should establish mRNA biodefense manufacturing as a priority — before America’s adversaries close the gap.

The Accelerating Threat

What once required advanced national laboratories — designing dangerous pathogens or engineering novel biological agents —can now be done with modest time and resources. Adversaries can design and deploy engineered threats in weeks, while traditional countermeasures can still take years to develop.

This widening gap — between the speed of potential attackers and the sluggishness of America’s defenses — is one of the most urgent national security challenges of our generation. And that gap continues to widen with each new technological advance.

Researchers recently created the first AI-designed viruses — bacteriophages that kill bacteria — using models trained on millions of viral genomes. Out of 302 computer-generated designs, 16 proved not only viable but superior to their natural counterparts.

These experiments were carried out under strict safeguards and for beneficial purposes. The bacteriophages targeted bacteria, not humans, and the researchers deliberately excluded human virus data from their AI training. However, the proof of concept is what matters. The underlying methods — training generative models on viral genomics — are becoming increasingly sophisticated and not limited to safe applications.

What now requires a sophisticated team of researchers will become accessible to smaller actors. What is technically challenging today will become operationally straightforward in the future. While the ability to weaponize these techniques is not imminent, the trajectory is clear. AI capabilities advance rapidly. Responsible planning requires preparing countermeasures before threats fully materialize — not after.

If the threat landscape is accelerating, our biodefense strategy should accelerate even faster. One way to stay ahead of emerging threats is mRNA technologies, which offer a powerful platform for rapid, adaptable, and scalable countermeasures.

During COVID-19, researchers quickly obtained the viral genetic sequence, providing everything needed to begin developing an mRNA vaccine. The vaccine was also designed quickly, even though it would still take clinical trials involving tens of thousands of patients to prove its safety and efficacy. Close coordination between the government and private sector under President Donald Trump’s leadership made the unthinkable possible.

The speed advantage of mRNA stems from its simplicity. mRNA therapies work with the body’s existing protein-making machinery. Instead of taking months to make a new therapy in labs, mRNA provides genetic instructions for cells to produce the protective protein that alerts the immune system. Because mRNA is a natural part of human biology, vaccine development is faster and easier. In fact, once a pathogen’s genetic sequence is known, the mRNA code can be designed in hours.

The same technology that enabled a rapid response during the pandemic can be decisive against engineered threats. Our national defense can operate on timelines matching the development of offensive weapons — saving American lives, including those of military servicemembers in wartime. Experience shows this isn’t an abstract concern.

Take the USS Kidd: In 2020, the U.S. destroyer was taken offline when SARS-CoV-2 infections spread through the crew. The incident demonstrates how biological threats can neutralize military personnel as effectively as kinetic weapons.

mRNA platforms offer a meaningful defensive advantage, but deterrence by denial in biodefense differs from its kinetic counterpart. The challenge is three-fold: detecting or identifying an attack before symptoms appear, developing a countermeasure against the specific threat, and deploying countermeasures under operational conditions.

mRNA technology addresses the second challenge decisively. Once the genome of a pathogen is sequenced, countermeasures can be designed in hours. Consider a carrier strike group with deployable mRNA synthesis capability. Even if an adversary achieves initial surprise, rapid countermeasure production limits the attack’s duration and military impact. Traditional countermeasure timelines were predictable — attackers could plan around a months-long development window with confidence. mRNA collapses that timeline unpredictably. Adversaries can no longer reliably estimate how long a biological attack will remain effective, undermining the operational calculus that makes such weapons attractive in the first place.

Detection and deployment are harder problems to solve. Incubation periods for biological agents can range from days to weeks, during which an attack may not be fully recognized. Administering vaccines or therapeutics in contested environments poses logistical challenges. Researchers, however, are making progress.

Unlike traditional vaccines dedicated to specific pathogens, mRNA manufacturing pivots rapidly between new countermeasures by changing only the RNA sequence — like updating software while keeping its hardware constant. Advances in miniaturization are moving toward deployable systems able to operate in forward bases or even battlefield conditions.

With continued federal investment and private-sector collaboration, these challenges can be addressed to better protect the American people and America’s warfighters. Yet just as the mRNA capability becomes essential and its expansion critical, the United States is retreating from it. In August, the U.S. Department of Health and Human Services discontinued approximately $500 million in mRNA research funding. The decision sent a chill through the biotechnology sector, undermining continued American innovation.

The $500 million cut represents more than a budget line — it has dismantled a coordinated research pipeline. The department’s mRNA research portfolio supported the development of multiple potential vaccines, manufacturing scale-up, and clinical trial infrastructure that no single defense contract replicates. These programs also operate on longer time horizons than typical defense procurement, sustaining the basic research and workforce development that private industry builds upon but rarely funds independently.

Defense funding alone cannot fill this gap. Biodefense programs funded through the U.S. Department of Defense are mission-specific and threat-focused. These programs procure capabilities rather than sustaining the broad research base that enables rapid pivots to new threats. For biodefense countermeasures, the federal government is the market. When the Biomedical Advanced Research and Development Authority (BARDA) stopped funding mRNA development, the signal to industry was clear: Move your resources elsewhere. The pre-pandemic mRNA ecosystem worked because civilian health agencies provided foundational research that both defense and commercial applications could draw upon.

Unless the federal government reverses course, the United States risks losing its hard-earned competitive advantage in a technology that enables an effective, timely response to future biological threats at precisely the moment our country can least afford to fall behind. Progress achieved through significant risk and taxpayer expense would be squandered.

Our global competitors are not making the same mistake. China has made significant investments in mRNA technology, with 46 percent of mRNA vaccines in clinical development globally now coming from China — a remarkable shift in a field where American firms held clear leadership just five years ago.

China is not merely trying to catch up but actively competing for dominance in a critical dual-use technology. In a biological crisis involving engineered threats, nations will either refuse to supply countermeasures to their adversaries or do so at great cost. Maintaining our leadership in mRNA research, development, and production is a national security imperative.

The decision to walk away from mRNA research comes at exactly the wrong moment. Former officials — including those who served under Trump — have said the move undermines deterrence and weakens national defense. While the U.S. Department of Defense continues funding some mRNA research, fragmentation of what was previously a coordinated civilian-military ecosystem threatens future progress and readiness.

Restoring this capability requires two complementary actions. First, Congress should restore the $500 million in lost mRNA research funding. This would not only help rebuild the civilian research base but send a strong message from Capitol Hill that policymakers understand the strategic value of mRNA technology. Second, the Department of Defense should establish a dedicated biodefense manufacturing initiative. The goal is not to replace efforts underway at other agencies, but to ensure continuity of surge capacity regardless of shifting civilian priorities. The Defense Department’s BioMADE program supports bioindustrial manufacturing — fuels, textiles, chemicals — but mRNA countermeasures require fundamentally different infrastructure. No current Defense Department program provides this capability.

Neither action alone is sufficient, but both are necessary to maintain American leadership in mRNA innovation and the integrated capability that the public and private sectors demonstrated under President Trump’s past leadership.

The mRNA technology necessary to face future biological threats already exists. Its strategic value is clear. The question facing policymakers and the American public is not whether engineered biological threats will emerge, but whether America will surrender this critical asset and be defenseless when they do.



Jeff Coller, PhD, is the Bloomberg distinguished professor of RNA biology and therapeutics at Johns Hopkins University. He is also co-founder of the Alliance for mRNA Medicines and co-founder of Tevard Biosciences.

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/covid-19-infection-quietly-speeds-up-artery-damage-or-atherosclerosis

(fair use applies)


COVID-19 Infection Quietly Speeds Up Artery Damage or Atherosclerosis
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 29, 2026

A growing body of evidence is now raising concerns that COVID-19 may leave behind more than short-term illness, potentially accelerating damage inside blood vessels long after recovery. New scientific commentary is drawing attention to subtle but important changes in arteries seen in people who have survived COVID-19, suggesting possible long-term heart and stroke risks.


What Prompted the New Concerns
The discussion centers on a recent study that examined whether COVID-19 infection could speed up early artery damage, a process known as atherosclerosis. This condition involves the gradual thickening of artery walls and is a major cause of heart attacks and strokes. Researchers focused on a measurement called carotid intima-media thickness, or CIMT, which looks at the thickness of the artery wall in the neck using ultrasound.

The study was by researchers from several institutions, including an independent research center in Basel Switzerland, the Department of Neurology at the National Memorial Hospital of Vukovar in Croatia, Sveti Duh University Hospital in Zagreb Croatia, and the Faculty of Medicine and Faculty of Dental Medicine and Health at the University Josip Juraj Strossmayer of Osijek Croatia.


Key Findings Explained Simply
The original study followed 92 adults, including people who had recovered from COVID-19 and a control group with no prior infection. At the start, artery thickness was similar in both groups. However, after 12 to 18 months, those who had COVID-19 showed a noticeably greater increase in artery wall thickness. In simple terms, their arteries appeared to age faster.

Blood tests revealed that higher levels of inflammation markers, such as C-reactive protein, and unhealthy fat ratios in the blood were linked to this faster artery thickening. Age and heart rate also played an important role in how quickly these changes occurred.


Why Measurement Accuracy Matters
The commentary highlights several technical issues that could influence how results are interpreted. Atherosclerosis does not develop evenly, and measuring only one small area of an artery may miss other problem spots. Timing measurements with the heartbeat is also critical, as artery thickness naturally changes during each beat. Without strict consistency, small errors can appear large, especially when changes are measured in fractions of a millimeter.

In addition, the authors stress the importance of using the same artery location during follow-up scans and ensuring that examiners are blinded to patient history to avoid unintentional bias.


Why This Medical News Report Matters
This Medical News report underscores that even mild or moderate COVID-19 infections may have hidden effects on the cardiovascular system. While CIMT testing is quick and non-invasive, it requires careful technique to produce reliable results. Small in accuracies could lead to misleading conclusions about heart risk.


Conclusions And Public Health Implications
The findings reinforce growing concerns that COVID-19 may trigger long-lasting inflammation that quietly damages blood vessels. Although more large-scale studies are needed, the evidence suggests survivors may benefit from cardiovascular monitoring. Understanding these risks early could help doctors prevent future heart attacks or strokes through lifestyle changes and targeted treatment strategies.

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

https://www.mdpi.com/1999-4915/18/2/170

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/long-covid-eye-pain-tied-to-hidden-nerve-dysfunction

(fair use applies)


Long COVID Eye Pain Tied to Hidden Nerve Dysfunction
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 29, 2026

Researchers from the Miami Veterans Administration Medical Center and the Bascom Palmer Eye Institute at the University of Miami in Florida USA have uncovered important evidence showing that persistent eye discomfort in long COVID patients may be closely linked to dysfunction of the autonomic nervous system, the part of the body that controls involuntary functions such as heart rate blood pressure tear production and pupil response.


Why Eye Symptoms Matter in Long COVID
Long COVID is known to affect multiple organs long after the initial infection clears. Many patients complain of fatigue dizziness heart palpitations and brain fog but eye symptoms are often overlooked. These include dryness burning light sensitivity and even sharp eye pain. This Medical News report highlights that such symptoms are not just local eye problems but may reflect deeper nerve system involvement.


Who Conducted The Study and Where
The study was carried out by researchers affiliated with the Surgical and Research Services at the Miami Veterans Administration Medical Center and the Bascom Palmer Eye Institute at the University of Miami. The research team analyzed data from 162 veterans diagnosed with long COVID who were treated at a specialized long COVID clinic.


How The Study Was Done
Participants completed detailed questionnaires measuring dry eye symptoms eye pain and features of nerve related pain such as sensitivity to light wind or temperature. Autonomic nervous system symptoms were assessed using a validated tool that measures issues like dizziness on standing sweating problems digestive complaints and visual disturbances. A subgroup of patients also underwent physical testing that measured changes in blood pressure heart rate and heart rate variability while lying down and standing.


Key Findings Explained Simply
More than three quarters of participants reported significant dry eye symptoms. Those with worse eye discomfort also had much higher scores for autonomic symptoms across almost all body systems. The strongest links were found between eye symptoms and pupillomotor problems which affect how the pupil responds to light and secretomotor problems which affect tear and saliva production. Importantly while clear cut diagnoses like postural tachycardia were uncommon subtle fluctuations in blood pressure and heart rate were strongly linked to eye pain especially pain triggered by heat cold or bright light. This suggests that eye pain in long COVID may behave like nerve pain rather than simple dryness.


What This Means for Patients and Doctors
The findings suggest that persistent eye pain and dryness may be warning signs of broader nerve instability in long COVID. Treating the eyes alone may not be enough if underlying autonomic dysfunction is not addressed. The study also helps explain why many patients have sev ere symptoms despite normal eye exams.


Conclusions And Future Directions
In conclusion this research shows that eye pain and dryness in long COVID are strongly connected to widespread autonomic nervous system symptoms and subtle cardiovascular instability. These findings support the idea that long COVID is a multisystem nerve related condition and that eye complaints should be taken seriously as part of the whole disease picture. Recognizing this connection may help guide more effective multidisciplinary treatment strategies and improve quality of life for long COVID sufferers.

The study findings were published in the peer reviewed journal: Brain Sciences

https://www.mdpi.com/2076-3425/16/2/135

 

[Heliobas Disciple]

https://medicalxpress.com/news/2026-01-metformin-shown-covid-groups-multiple.html

(fair use applies)


Metformin shown to prevent long COVID across risk groups in multiple randomized trials
by University of Minnesota Medical School
edited by Stephanie Baum, reviewed by Andrew Zinin
The GIST
January 29, 2026

Multiple randomized clinical trials and electronic health record studies now show that metformin, a widely used and well-established medication, significantly reduces the risk of developing long COVID when taken during or shortly after acute infection with SARS-CoV-2. The findings are published in Clinical Infectious Diseases.

In the paper, the University of Minnesota Medical School research team provides information about metformin and summarizes several studies in low, standard and high risk populations that show taking metformin during or soon after infection with SARS-CoV-2 prevents the development of long COVID. Notably, the research summarizes the number of patients needed to receive treatment in each study to prevent one case of long COVID. On average across the four studies, one case of long COVID is prevented for every 50 cases of acute SARS-CoV-2 treated with 14 days of metformin.

"Metformin has emerged as the first intervention to prevent long COVID in low to high risk adults and across multiple clinical trials and high-quality electronic health record studies," said Carolyn Bramante, MD, MPH, an assistant professor at the University of Minnesota Medical School and physician with M Health Fairview. "This body of evidence means that starting metformin at the time of infection can reduce the risk of long COVID for most adults who get COVID-19 today."

Other key findings from the literature on using metformin to treat an acute infection:

• Compared to placebo, metformin significantly decreases SARS-CoV-2 viral load and prevents rebound of viral load.
• Metformin is the first intervention to be tested in two large, placebo-controlled, randomized trials in low-, standard-, and high-risk adults, including adults with prior infection for preventing long COVID.
• Two of these research studies included persons who were also given FDA-approved treatments of SARS- COV-2 (including nirmatrelvir-ritonavir, molnupiravir, and remdesivir).
• Most adults can take metformin, but should ask their clinician.
• Metformin during acute COVID-19 is safe and does not cause low blood sugar or serious side effects.

The conclusion from these four studies—that treating SARS-CoV-2 with 14 days of metformin can prevent long COVID—applies to most adults being infected with COVID-19 in the current state of the pandemic. The research team also notes that metformin can be used alone or combined with other treatments for acute SARS-CoV-2.

It is not known whether metformin can prevent long COVID in pediatric populations, nor if metformin treats long COVID in either adults or pediatric populations.

Publication details
Carolyn T. Bramante et al, Preventing Long COVID With Metformin, Clinical Infectious Diseases (2026). DOI: 10.1093/cid/ciaf700
Journal information: Clinical Infectious Diseases
Provided by University of Minnesota Medical School

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/long-covid-smell-loss-may-signal-future-memory-decline

(fair use applies)


Long COVID Smell Loss May Signal Future Memory Decline
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 30, 2026

A growing body of scientific evidence is raising fresh concerns that the loss of smell experienced by many COVID-19 survivors may be more than a temporary nuisance and could be an early warning sign of future cognitive decline and Alzheimer’s disease.

Researchers from Fondazione Policlinico Universitario Agostino Gemelli IRCCS in Rome, Ospedale Isola Tiberina Gemelli Isola in Rome, the European Brain Research Institute EBRI in Rome, and the Institute of Translational Pharmacology of the Italian National Research Council have conducted an extensive review examining how long-lasting smell impairment after SARS-CoV-2 infection may affect the brain.


Why Smell Loss Matters More Than People Realize
Loss of smell, medically known as anosmia, affects a large proportion of people with long COVID. While many regain their sense of smell within weeks, a significant number experience persistent or even permanent impairment. Scientists emphasize that the sense of smell is directly connected to brain regions responsible for memory, emotions, and learning, including the hippocampus and limbic system. Damage along these pathways can therefore have far-reaching consequences beyond the nose.


How the Virus Triggers Brain Changes
The study explains that SARS-CoV-2 does not usually infect smell-sensing neurons directly. Instead, it damages supporting cells in the nasal lining and triggers chronic inflammation. This prolonged immune response disrupts normal regeneration of the olfactory system and may lead to shrinkage of the olfactory bulbs, the brain’s first relay station for smell. Over time, these changes can ripple into deeper brain structures involved in thinking and memory.


Links to Cognitive Decline and Alzheimer’s Disease
Multiple clinical studies reviewed by the researchers show that people with persistent smell loss after COVID-19 often perform worse on memory and cognitive tests. Brain scans from long COVID patients have revealed thinning of brain regions associated with memory and decision-making. Importantly, smell impairment is already known to be one of the earliest signs of Alzheimer’s disease, sometimes appearing years before noticeable memory loss.

This Medical News report highlights that inflammation, oxidative stress, and abnormal protein buildup triggered by SARS-CoV-2 closely resemble processes seen in Alzheimer’s disease. These shared mechanisms raise the possibility that COVID-19 may accelerate underlying neurodegenerative changes in vulnerable individuals, particularly older adults.


Treatment and Prevention Strategies
The researchers stress the importance of early intervention. Olfactory training, which involves repeated exposure to specific scents, along with anti-inflammatory and neuroprotective treatments, may help restore smell function and potentially reduce long-term brain risks. Monitoring smell loss could also become a simple and cost-effective way to identify people who may need closer neurological follow-up.


Conclusions and Public Health Implications
The findings strongly suggest that persistent smell loss after COVID-19 should not be ignored or dismissed as harmless. Instead, it may serve as an early biological signal of brain vulnerability and future cognitive decline. Long-term studies are still needed, but current evidence supports routine assessment of olfactory function as part of post-COVID care, especially for older adults and those with lingering symptoms.

The study findings were published in the peer reviewed journal: Cells

https://www.mdpi.com/2073-4409/15/2/176

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/old-cough-drug-shows-power-against-new-covid-19-variants

(fair use applies)


Old Cough Drug Shows Power Against New COVID-19 Variants
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 30, 2026

A team of scientists from Chile has uncovered promising new evidence that a long-used cough medication may help block infection from COVID-19 variants, including Omicron. The research suggests that bromhexine, a drug commonly prescribed for respiratory conditions such as coughs, can interfere with the virus at the earliest stage of infection, before it even enters human cells.


Researchers And Institutions Involved
The study was conducted by researchers from the Laboratorio de Fisiología Molecular, Facultad de Medicina, Universidad de Talca; the Departamento de Medicina Traslacional, Facultad de Medicina, Universidad Católica del Maule; the Departamento de Farmacología, Facultad de Ciencias Biológicas, Universidad de Concepción; the Center for Nanomedicine Diagnostic and Drug Development at Universidad de Talca; and the Center for the Development of Nanoscience and Nanotechnology CEDENNA in Chile.


Why Blocking Viral Entry Matters
COVID-19 begins when the virus attaches itself to a protein called ACE2 found on the surface of human cells. Once attached, the virus slips inside and starts multiplying. Many treatments focus on stopping the virus after infection has already occurred. However, blocking this first step could prevent illness altogether. This Medical News report highlights how bromhexine may disrupt that crucial attachment process.


How The Study Was Carried Out
Instead of using live coronavirus, the researchers used a safe laboratory model known as a pseudovirus. This model mimics the behavior of real SARS-CoV-2 but cannot reproduce or cause disease. Human kidney cells were genetically modified to carry large amounts of the ACE2 receptor, making them ideal for studying viral entry. The cells were then exposed to Omicron and other variant pseudoviruses after being treated with different doses of bromhexine.


Key Findings Explained Simply
The results were striking. Bromhexine reduced Omicron variant infection by about sixty percent at higher doses. Even at lower concentrations, it cut viral entry in half, with an effective inhibitory dose measured at around 17 micromolar. When tested against Alpha, Beta, and Delta variants, bromhexine still reduced infection by roughly forty percent, suggesting it works broadly across multiple variants.

Computer simulations revealed why this happens. Bromhexine was shown to bind tightly to the ACE2 receptor at specific sites. By attaching there, the drug destabilizes the contact point where the virus normally locks on, making it much harder for the virus to enter cells.


Why This Discovery Is Important
Bromhexine is inexpensive, widely available, and already approved for use in humans. This makes it an attractive candidate for drug repurposing, especially in regions where access to new antivirals is limited. Because it targets a human receptor rather than the virus itself, it may remain effective even as new variants emerge.


Conclusion
The findings strongly suggest that bromhexine could serve as a frontline defense against COVID-19 by blocking viral entry at the cellular level. While further studies using live virus and clinical trials in humans are still required, the evidence supports bromhexine’s potential role as an early-stage therapeutic option, particularly when combined with other antiviral strategies. Its affordability and global availability further strengthen its relevance in ongoing and future pandemic responses.

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

Frontiers | Bromhexine inhibits SARS-CoV-2 Omicron and variant pseudovirus infection via ACE2-targeted mechanisms

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) causes a highly infectious disease characterized by fever, acute respiratory illness, ...

www.frontiersin.org

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/hidden-viral-trick-that-helps-covid-19-outsmart-immunity

(fair use applies)


Hidden Viral Trick That Helps COVID-19 Outsmart Immunity
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 01, 2026

A new scientific study has uncovered an unexpected and troubling way the SARS-CoV-2 virus may be protecting itself from the human immune system, helping to explain why COVID-19 can sometimes become severe and prolonged. The research reveals that a key viral component, known as the nucleocapsid protein, can hijack natural immune regulators in the blood and use them as a shield against immune attack.

This Medical News report highlights findings from researchers based at the Laboratory of Biomedical Microbiology and Immunology, University of Veterinary Medicine and Pharmacy in Košice, Slovakia, and the Institute of Neuroimmunology, Slovak Academy of Sciences in Bratislava, Slovakia.


Understanding the Immune System Targeted by the Virus
The human body relies on the complement system, a powerful part of innate immunity made up of more than 30 proteins, to quickly identify and destroy invading microbes. When working properly, this system punches holes in viruses, marks them for destruction, and prevents infection from spreading.

To avoid harming healthy cells, the complement system is tightly controlled by special molecules called complement regulatory proteins. These regulators act like brakes, ensuring the immune response does not get out of hand.


The Viral Protein That Plays a Double Role
The SARS-CoV-2 nucleocapsid protein, commonly called the N-protein, is best known for packaging the virus’s genetic material. However, the study found that this protein does much more. Large amounts of N-protein are released into the bloodstream of infected individuals, especially those with severe COVID-19.

The researchers discovered that the N-protein strongly binds to several major complement regulatory proteins, including C1 inhibitor, C4 binding protein, factor H, and vitronectin. These are the very molecules meant to protect human cells from immune damage.


How the Virus Uses Human Defenses Against Us
Crucially, the study showed that while the viral spike protein alone could not attract these immune regulators, the N-protein could act as a bridge. The N-protein binds to the spike protein on the virus surface and simultaneously captures complement regulatory proteins from human blood.

This creates a three-part complex where the virus becomes coated with human immune regulators. As a result, the virus may appear more like a normal human cell to the immune system, allowing it to slip past immune defenses.


Blocking the Body’s Final Line of Attack
One of the most alarming findings was that the N-protein reduced formation of the membrane attack complex, a structure that normally destroys viruses by punching lethal holes in them. When N-protein levels were higher, this destructive immune mechanism was significantly weakened.

This suggests that SARS-CoV-2 may actively dampen immune killing while circulating in the bloodstream, giving it more time to spread and cause damage.


Why This Matters for Severe COVID-19
High levels of N-protein in blood have already been linked to worse disease outcomes. This study provides a clear biological explanation for that link. By recruiting immune regulators, the virus may both avoid destruction and contribute to immune imbalance, which is often seen in severe COVID-19 cases.


Conclusions
The findings reveal a sophisticated immune evasion strategy used by SARS-CoV-2 that goes beyond what was previously known. The nucleocapsid protein appears to function as a molecular adaptor, allowing the virus to cloak itself with human immune regulatory proteins and weaken the complement system. This mechanism may help explain persistent viral presence, immune dysregulation, and severe disease outcomes in some patients. Understanding this interaction opens new possibilities for treatments that block N-protein interactions, restore proper immune function, and reduce severe COVID-19 complications.

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

SARS-CoV-2 nucleocapsid protein forms complexes with soluble complement regulatory proteins that can bind to the virion - Scientific Reports

The SARS-CoV-2 nucleocapsid protein has been detected in the plasma of COVID-19 patients, and its levels in the plasma correlate with the severity of the disease. It is also an immunomodulatory protein, triggering the release of proinflammatory cytokines. Complement system dysregulation in...

link.springer.com

 

[Heliobas Disciple]

I need some help with this post! I don't have a twitter account so I can't see Geert's response to the tweet that he's directing people to see. If someone can post his reply that would be great. thanks.

The currently observed metastable expansion of BA.3.2 (sub)lineages reflects not resolution but exhaustion of conventional evolutionary pathways, priming a dangerous qualitative phase transition!

please find my comments to Stefan Pöhlmann’s post on X (with all my respect for Stefan’s work; he’s keeping us updated on the evolutionary path of SC-2, especially re: BA.3.2 (sub)variants):

voiceforscienceandsolidarity.substack.com

(fair use applies)


The currently observed metastable expansion of BA.3.2 (sub)lineages reflects not resolution but exhaustion of conventional evolutionary pathways, priming a dangerous qualitative phase transition!
Geert Vanden Bossche
Feb 04, 2026

please find my comments to Stefan Pöhlmann’s post on X (with all my respect for Stefan’s work; he’s keeping us updated on the evolutionary path of SC-2, especially re: BA.3.2 (sub)variants):

https://x.com/snpoehlm/status/2018091814851362909

Stefan Pöhlmann@snpoehlm
5:39 PM · Feb 1, 2026

BA.3.2 might mark a step towards endemic coronaviruses rather than the next dominant variant.

https://x.com/JPWeiland/status/2018064775402418584

JWeiland @JPWeiland​

3:51 PM · Feb 1, 2026​

​

BA.3.2 is behaving differently than any of the other variants we've seen.​

​

I've been wondering for some time if this is our first example of co-circulation, where only part of the population is susceptable to infection. It is starting to look stabilized in Germany, not a sweep.​

​

​

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/new-sars-cov-2-mutants-tricks-the-human-host-on-multiple-fronts

(fair use applies)


New SARS-CoV-2 Mutants Tricks the Human Host on Multiple Fronts
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 02, 2026


Medical News: Scientists Warn Virus Evolution Far from Over
A sweeping new review warns that SARS-CoV-2—the coronavirus behind COVID-19—continues to shift, strengthen and change how it attacks the human body years after the original outbreak. The research was conducted by teams from George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mure? and the Clinical County Hospital of Mure?, Romania, with contributions from units including the university’s Departments of Pneumology, Pathophysiology, Genetics, Clinical Laboratory, and Plastic and Reconstructive Microsurgery.


Constant mutations make the virus harder to predict
Although the pandemic emergency has ended, scientists say the virus is still adapting rapidly. The review found that new Omicron descendants—including BA.2.86, JN.1 and the KP variants—carry mutations that allow them to latch onto human cells more tightly, slip past antibodies and exploit weaknesses in the immune system. Researchers explain that genetic tweaks in the spike protein change how the virus grabs the ACE2 receptor, with mutations such as L455F boosting binding strength and others like H146K and I210T helping variants evade immune recognition.


Hidden entry routes help infection spread
The review also reveals that the coronavirus now uses more than one doorway to invade cells. Besides ACE2, it relies on cell enzymes such as TMPRSS2 and even backup entry helpers like neuropilin-1, found in the lungs, liver, heart and nerve cells. This Medical News report notes that neuropilin-1 is especially worrying because it is found in organs that continue to be damaged by the virus, even when respiratory symptoms fade.


Once inside the body the virus rewires cells
After attaching to cells, SARS-CoV-2 forces the host machinery to copy its genetic code and build new virus particles. A crucial viral enzyme called nsp14 edits errors in viral RNA while helping camouflage it from immune alarms. The study highlights that even small changes in nsp14 can dramatically alter viral survival, mutation rates and the virus’s ability to resist antiviral drugs.


Multi organ damage supported by powerful omics data
The scientists warn that internal injury does not stem only from the virus multiplying but from how it disturbs normal cell chemistry.

• Heart: Blood samples from myocarditis patients showed high levels of TNF-related inflammation and mitochondrial stress, suggesting energy collapse inside heart muscle cells.

• Liver: Clusters of aggressive CD8 T cells were found sitting directly next to liver cells, armed with tissue-destroying enzymes.

• Kidneys: Severe COVID-related acute kidney injury was linked to failing cellular energy systems and burned-out metabolic pathways, unlike typical sepsis-related kidney failure.

These discoveries come from advanced tools such as spatial transcriptomics, which show where cells are altered inside organs, and proteomics, which measures thousands of proteins simultaneously.


What it all means moving forward
The SARS-CoV-2 virus is learning how to sidestep neutralizing antibodies and may be slowly pressuring T-cell defenses as well. The authors stress that next-generation vaccines must include components that do not mutate frequently, such as parts of the spike’s S2 region and internal viral proteins. They also argue that therapies that support cell metabolism—mitochondria, stress pathways and inflammation control—may help prevent long-term damage.


Conclusion
The study concludes that SARS-CoV-2 continues to evolve in ways that reshape infection, immune escape and organ disease. Its success comes from a powerful combination of structural mutations, immune suppression tools, and the ability to reprogram metabolism inside infected tissues. Scientists emphasize that staying ahead of future variants will require global surveillance, smarter vaccines and treatments that also target the host pathways the virus hijacks. Only with this two-pronged approach can health systems remain prepared for future waves and long-term COVID complications.

The study findings were published in the peer reviewed International Journal of Molecular Sciences.

https://www.mdpi.com/1422-0067/27/2/891

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/covid-19-quietly-alters-heart-function-in-survivors

(fair use applies)


COVID-19 Quietly Alters Heart Function in Survivors
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 02, 2026


Medical News: Subtle Heart Changes Emerging After COVID-19 Recovery
As the world continues to grapple with the long-term effects of COVID-19, scientists are uncovering growing evidence that the virus may leave behind quiet but measurable changes in heart function. A new large-scale analysis now suggests that many people suffering from Long COVID experience subtle heart performance issues, even months after their initial infection has resolved.

This Medical News report focuses on a comprehensive systematic review and advanced meta-analysis that examined how post-acute sequelae of COVID-19, commonly known as Long COVID, affect the structure and function of the heart.


Who Conducted The Research
The study was led by researchers from the Baker Heart and Diabetes Institute and the University of Melbourne in Australia, with additional contributions from Monash University in Australia, the Federal University of Goiás in Brazil, Perspectum Diagnostics in the United Kingdom, University College London in the United Kingdom, and the University of Tasmania in Australia.


How The Study Was Carried Out
Researchers analyzed data from 17 previous clinical studies involving 4,852 adults, including more than 3,100 individuals diagnosed with Long COVID. Advanced heart imaging methods such as echocardiography and cardiac MRI were used to evaluate heart structure and performance. The research team also gained access to detailed participant-level data from three studies, allowing deeper analysis of individual heart measurements.


Key Findings on Heart Function
One of the most important findings involved a measure known as global longitudinal strain, which detects early and subtle heart muscle weakness. Over half of Long COVID patients showed abnormal strain values, compared to only a small fraction of people without lingering symptoms. This suggests hidden heart muscle impairment that may not show up on routine tests.

The study also found small reductions in left ventricular ejection fraction, a standard measure of how efficiently the heart pumps blood. While these changes were modest and often remained within normal ranges, they consistently appeared more often in people with Long COVID than in control groups.


Who Is Most At Risk
Older adults and individuals with pre-existing conditions such as diabetes or high blood pressure showed more pronounced heart changes. These groups appeared more vulnerable to subtle heart dysfunction after COVID-19, highlighting the importance of targeted monitoring rather than blanket testing for all survivors.


Structural Changes Were Mild
Interestingly, major structural heart changes were uncommon. Most heart chambers remained normal in size, and right-sided heart function showed little difference between Long COVID patients and controls. This re inforces the idea that Long COVID-related heart effects are often functional rather than structural.


Why These Findings Matter
Although the detected heart changes are usually mild, researchers warn that even small impairments could add up over time, especially in people with other health risks. These findings suggest that Long COVID may quietly increase future cardiovascular vulnerability in certain populations.


Conclusion
Overall, the study shows that Long COVID is linked to modest but consistent reductions in heart performance, particularly affecting how the left side of the heart contracts. While these changes are often subclinical, they may carry long-term implications for cardiovascular health, especially among older adults and those with metabolic conditions. Careful, risk-based follow-up rather than routine heart screening for everyone with Long COVID appears to be the most sensible approach moving forward.

The study findings were published in the peer reviewed American Journal of Preventive Cardiology.

https://www.sciencedirect.com/science/article/pii/S2666667726000516

 

[psychgirl]

Slight change of topic; I’ve not been keeping up with the COVID posts lately and apologize but my house has been busy with DH knee surgery recovery and yes….viral illness all at the same time

He’s going through both. I’ve been fighting not feeling well for two months.

I have to mention that this current “cold bug/virus” chest and head infection that’s circulating is absolutely horrible.
It’s almost as bad as a Covid infection!

Drags on and on with multiple rounds of differing symptoms that linger for weeks. This one just feels different. And please, be very careful if you have a tendency for infections to go into the lungs because this one is a bear!

I was hoping there’s more information regarding this “cold” but really haven’t seen anything (?) People reporting they have this nasty bug all say the same things.

 

[Zoner]

https://twitter.com/i/web/status/2018977086036132218

View: https://twitter.com/gvdbossche/status/2018977086036132218?s=46&t=1GPp52vDMcboAD8_ZMiCSw

 

[Heliobas Disciple]

https://twitter.com/i/web/status/2018977086036132218

View: https://twitter.com/gvdbossche/status/2018977086036132218?s=46&t=1GPp52vDMcboAD8_ZMiCSw

Thank you!!!!!

I will post the text in case the tweet disappears, adding my own paragraph breaks to make it easier to read:

Geert Vanden Bossche @GVDBossche
4:17 AM · Feb 4, 2026

I am not sure I agree!

The behavior of BA.3.2 is not consistent with endemic stabilization or ‘partial susceptibility,’ but with escalating immune constraint! A true endemic equilibrium would not require this extensive mutational effort (>50 mutations in S alone!).

In highly C-19 vaccinated populations, susceptibility is dynamic, not compartmentalized, and true partial susceptibility would rapidly collapse into either a selective sweep or extinction of SARS-CoV-2, not just co-circulation! Instead, BA.3.2 shows slow or stagnating, but persistent expansion, extensive S remodeling, strong convergent evolution, and yet no decisive growth advantage-a typical evolutionary signature of constraint, not endemic stabilization!

Such high mutational effort for marginal phenotypic gain indicates that further improvement via amino-acid substitution has become sterically and functionally limited under population-level immune pressure on transmissibility (exerted by highly C-19-vaccinated populations!).

The resulting metastable plateau below dominance is therefore best interpreted as an evolutionary dead-end behavior, i.e., a hallmark of a system nearing the threshold to a phase transition, not an endemic equilibrium! In this context, stabilization does not reflect resolution but exhaustion of conventional evolutionary mutations, setting the stage for a dangerous qualitative phase transition rather than benign co-circulation:

Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape

The absence of worsening clinical signals during the emergence of newly circulating variants does not imply intrinsic attenuation of SARS-CoV-2 (SC-2) or its transition toward endemicity but instead sets the stage for the selection of additional, virulence-enabling O-glycosylation as last-resort...

www.trialsitenews.com

 

[Heliobas Disciple]

MORE FROM GEERT. HE POSTED TWO TIMES TODAY - THE FIRST IS THE MORE SCIENTIFIC POST AND THE SECOND IS THE SAME ARTICLE MADE EASIER TO READ FOR 'LAYPEOPLE' (ie: folks like us!). I WILL POST BOTH.

Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst...

Introduction

voiceforscienceandsolidarity.substack.com

(fair use applies)


Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst...
Geert Vanden Bossche
Feb 07, 2026

Introduction

Waste water data on viral load across different states in the US or highly C-19 vaccinated countries show ongoing community circulation of SARS-CoV-2 (SC-2), despite low reported symptom-based cases.

Because so many people no longer get tested when they feel sick, or experience asymptomatic infections, traditional Covid case counts have become less reliable. That’s where wastewater testing comes in. The latest wastewater data show that viral RNA continues to show up in wastewater, and in some places viral load is increasing compared to recent weeks. This means the virus is still circulating in the community, even if we don’t see big clinical waves.

While current wastewater reporting doesn’t always identify specific variants (like BA.3.2) by name, the continued virus signal tells us transmission is happening behind the scenes. Those following Covid-19 news on X will be aware that genomic wastewater surveillance notes BA.3.2 (sub)lineages (co-)circulating in a steadily increasing number of highly C-19-vaccinated countries.

As explained below, this pattern -silent (co)circulation of pre-existing and newly emerging SC-2 lineages with modest clinical impact- is precisely what my theory predicts at near-threshold immune pressure exerted by highly C-19-vaccinated populations.

Clearly, the virus is not going away and its presence is only poorly captured by standard testing patterns or traditional case counts, yet it’s clearly there, spreading and exchanging many mutations to adapt to its ‘hostile’ immune environment. However, it does so quietly, constrained by that immune environment, thereby limiting explosive disease outbreaks.

Data-to-Theory: How current BA.3.2 (‘Cicada’) dynamics in highly C-19-vaccinated populations align with a near-threshold evolutionary pathway

Recent genomic, epidemiological, and clinical surveillance data reveal an evolutionary pattern in BA.3.2-derived SC-2 lineages that is difficult to reconcile with classical models of simple directional selection toward higher intrinsic transmissibility or attenuation. Instead, the observed dynamics are more consistent with viral evolution under escalating population-level immune pressure acting on the phenotype of transmissibility, precisely the regime predicted to precede a qualitative evolutionary phase transition (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape).

1. Genomic surveillance: high mutational effort, limited phenotypic return

BA.3.2 and its descendants (e.g., RE.1.1, RE.2.2) are among the most divergent Omicron-related lineages observed to date, carrying dozens of Spike (S) mutations, with extensive remodeling of both the S-RBD and S-NTD (receptor-binding and N-terminal domain of S protein, respectively). In a classical fitness landscape, such extensive amino-acid remodeling would be expected either to confer a decisive growth advantage (leading to rapid sweeps) or to incur sufficient fitness cost to drive extinction. Neither outcome is observed!

Instead, BA.3.2-derived lineages persist and expand slowly and steadily, often within a narrow prevalence range and without consistent global dominance. This combination, i.e., large mutational diversity without clear fitness superiority, is a hallmark of constraint-dominated evolution, not optimization. It suggests that further gains in intrinsic transmissibility via incremental amino-acid substitutions are becoming increasingly sterically and functionally constrained.

2. Convergence without sweeping: a signature of narrowing solution space

Across multiple co-circulating lineages, there is increasing evidence of convergent acquisition of overlapping transmission-associated mutations, particularly in S domains linked to receptor engagement and antibody interaction. At the same time, displacement dynamics have slowed: variants coexist longer, and clean selective sweeps have become rarer.

Such convergence is expected when population-level immune pressure narrows the set of viable phenotypic solutions, forcing evolution onto a small number of shared mutational paths.

This pattern is inconsistent with benign endemic stabilization and instead signals an evolutionary system approaching a fitness bottleneck.

3. Epidemiology and wastewater: persistence without obvious clinical escalation

Where wastewater surveillance remains available, baseline SC-2 signal often remains elevated despite muted or delayed clinical peaks, consistent with immune-constrained replication rather than loss of viral viability. Importantly, the expansion of BA.3.2-derived (sub)lineages has not yet been associated with marked changes in population-level clinical severity.

In the proposed framework, this clinical neutrality is not reassuring; rather, it is expected during a pre-transition metastable phase, in which the virus accumulates extensive molecular change while phenotypic expression remains buffered…until a threshold is crossed.

4. Interpretation: near-threshold behavior, not endemic stabilization

Taken together, the slow expansion, lack of decisive growth advantage, extensive S remodeling and increasing mutational convergence of BA.3.2-derived lineages are difficult to explain by a model of gradual attenuation or simple directional selection. Instead, they are logically consistent with a virus evolving under escalating population-level immune pressure on transmissibility, where conventional amino-acid–based adaptation yields diminishing returns.

In such a regime, evolutionary theory predicts that qualitative rather than incremental adaptive shifts become selectively favored. In the context of SC-2, this provides a coherent rationale for why selection may eventually favor a glycosylation-driven phase transition that decouples viral spread from classical antigen presentation and immune-mediated clearance, rather than continued stepwise mutation (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape).

5. What this does-and does not-demonstrate

These observations do not prove that a phase transition has already occurred, nor do they uniquely establish the specific molecular mechanism by which I anticipate such phase transition to unfold (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape). However, they do profoundly undermine interpretations that frame BA.3.2 behavior as evidence of benign endemicity or evolutionary ‘settling.’ Instead, the current data are fully compatible with a near-threshold evolutionary state, in which the virus remains metastable while the remaining adaptive solution space continues to contract (TrialSiteNews | Independent Censorship-Free Media for Health & Biomedical Research https://voiceforscienceandsolidarity.substack.com/p/a-pandemic-panic-for-two-mutations; Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape).

In view of these considerations, BA.3.2-derived lineages should not be viewed as evolutionary endpoints but rather as diagnostic indicators of mounting immune constraint-conditions under which a sudden, qualitatively different evolutionary outcome becomes increasingly plausible.

 

[Heliobas Disciple]

Lay summary on recent Substack article: "Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst..."

For those who find it too challenging to read my recent Substack article (https://voiceforscienceandsolidarity.substack.com/publish/post/187208072), here follows a two-page lay summary:

voiceforscienceandsolidarity.substack.com

(fair use applies)

EMPHASIS MINE


Lay summary on recent Substack article: "Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst..."
Geert Vanden Bossche
Feb 07, 2026

For those who find it too challenging to read my recent Substack article, here follows a two-page lay summary:

Once again, this immune-escape pandemic confronts us with an unprecedented situation, one that is highly worrisome, yet not taken seriously by public health authorities and so-called experts.

Below, I’ll list the most remarkable features of the currently observed viral evolutionary dynamics, which primarily pertain to BA.3.2 and its offshoots. Most of this is redundant with what I described in previous Substacks or TSN articles, but repetitio est mater studiorum!

1. Business as unusual!

When scientists look at how new SARS-CoV-2 (SC-2) variants behave, they usually expect one of two things to happen:

Either a new variant spreads much faster and quickly replaces others,

Or it fails to compete and disappears.

What the current data tell us about BA.3.2 (also called Cicada) fits neither pattern:

2. Many changes, little payoff

BA.3.2 and its offshoots carry an unusually large number of changes in the spike (S)-protein, far more than most earlier variants. Normally, that many changes would either make a virus clearly stronger or clearly weaker. Instead, BA.3.2 is spreading slowly but persistently, without taking over completely and without disappearing! That’s totally unusual. It suggests the virus is working very hard and making many changes to adapt to its ‘hostile’ immune environment but getting only small gains in return. This usually means it’s facing some limitations, not smoothly improving.

3. Different variants making the same changes

Another striking pattern is that different variants are independently picking up similar mutations, especially ones linked to how the virus spreads and avoids immunity. This is called convergent evolution; it usually happens when the virus has very few remaining options that still work.

In simple terms: the virus is being pushed into a corner and keeps trying the same few tricks because most other options no longer help.

4. No big clinical changes…yet!

Despite all these mutations, BA.3.2 hasn’t caused a sudden jump in severe disease. Wastewater data and testing still show the virus (co-)circulating, but without dramatic new waves of illness or hospitalization. This may sound reassuring, but in this framework of limited viability options, that’s actually expected. Before a system undergoes a sudden shift, it often enters a metastable (i.e., stable-looking) phase where immune pressure keeps building beneath the surface.

Think of it like a fault line before an earthquake: things look calm, even though stress is accumulating. Or consider a pus-filled abscess: the skin still looks largely intact, even as pus builds up and exerts mounting pressure beneath it.

5. Why doesn’t this look like ‘endemic calm’?

Some people interpret BA.3.2’s slow, steady behavior as a sign that the SC-2 immune escape pandemic is settling down into something harmless and endemic. But that interpretation ignores an important detail: If the virus were simply stabilizing, it wouldn’t need to keep piling up mutations across its S protein just to maintain its position!

Instead, what we see -many mutations, slow growth, lots of overlap between co-circulating variants- fits better with a virus under strong immune pressure, struggling to keep adapting and spreading in a population with widespread vaccine-induced immunity.

6. What this means going forward

This pattern doesn’t prove that a sudden change will happen tomorrow. But it does suggest that the virus is approaching a breaking point, where small tweaks are no longer enough to ensure its survival.

When that happens in biology, evolution often takes a different kind of path, not a gradual one. My concern here is the virus transitioning to a behavior that enables spread by completely sidestepping adaptive, vaccine-primed immune defenses - rather than continuing to slowly mutate its S protein.

Conclusion

BA.3.2 is unlikely to be the final, ‘settled’ form of the virus. Its behavior looks more like a warning sign than an endpoint: a virus adapting under increasing immune pressure, with fewer and fewer workable options left.

I agree there is no evidence-based proof that the currently observed viral dynamics will inevitably lead to disaster, as we’re sailing uncharted waters. But it does mean that treating the current situation as boring, stable, or safely ‘endemic’ is reckless and unsupported by the data.

 

[Heliobas Disciple]

Same feed, different fleas: why BA.3.2 looks different across highly Covid-19-vaccinated countries without being benign!

We currently observe highly divergent trends in the viral evolutionary dynamics of BA.3.2 across distinct, highly Covid-19 (C-19)-vaccinated countries.

voiceforscienceandsolidarity.substack.com

(fair use applies)


Same feed, different fleas: why BA.3.2 looks different across highly Covid-19-vaccinated countries without being benign!
Geert Vanden Bossche
Feb 08, 2026

We currently observe highly divergent trends in the viral evolutionary dynamics of BA.3.2 across distinct, highly Covid-19 (C-19)-vaccinated countries. I commented on this observation reported on X as follows:

https://x.com/GVDBossche/status/2020427259539071291

“BA.3.2 sublineages most likely reflect a metastable state under near-threshold immune pressure. Under such a scenario, heterogeneous and fluctuating detection rates across highly C-19-vaccinated countries are not only expected- they are totally consistent with a system approaching a qualitative evolutionary transition rather than endemic stabilization!”​

What the title of this article really means is that what appear to be different viral evolutionary ‘behaviors’ across countries are actually surface variations on the same underlying immune pressure and calling these behaviors ‘benign’ doesn’t make them stable or ‘endemic’!

If BA.3.2-derived sublineages indeed reflect a metastable, near-threshold state of SARS-CoV-2 evolution in highly C-19-vaccinated populations rather than a lineage undergoing classical directional selection, then fluctuating detection rates across countries are not anomalous but indeed expected.

Under such a scenario, population-level immune pressure acts on the phenotype of transmissibility rather than on individual epitopes, rendering viral fitness highly sensitive to small changes in population-level immune pressure, driven by factors such as the rate and timing of vaccination (including booster doses) and (asymptomatic) vaccine breakthrough reinfection. Minor differences in public health policies and social behavior[1] leading to small differences in country-specific immune-history homogenization can therefore produce disproportionate swings in prevalence, thereby causing asynchronous rises and declines of BA.3.2 across otherwise comparable populations.

This instability is further amplified by competition within a severely constrained evolutionary solution space, where multiple lineages explore similar mutational neighborhoods but fail to achieve decisive fitness superiority. As a result, BA.3.2-derived sublineages may repeatedly gain and lose relative prevalence without sweeping to dominance, while remaining decoupled from major clinical signals.

Such fluctuating, non-monotonic behavior is a hallmark of systems approaching an evolutionary bottleneck and is more consistent with proximity to a qualitative phase transition than with benign endemic stabilization or evolutionary stasis (see previous Substack article: Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst...).

[1] This last factor is an extremely popular ‘scapegoat’ among public health authorities and so-called experts, mostly used inappropriately to explain whatever pandemic evolution, even when it follows a consistent course across different highly C-19 vaccinated populations.




~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Lay Summary on: "Same feed, different fleas: why BA.3.2 looks different across highly Covid-19-vaccinated countries without being benign!"

We currently observe highly divergent trends in the viral evolutionary dynamics of BA.3.2 across distinct, highly Covid-19 (C-19)-vaccinated countries.

voiceforscienceandsolidarity.substack.com

(fair use applies)


Lay Summary on: "Same feed, different fleas: why BA.3.2 looks different across highly Covid-19-vaccinated countries without being benign!"
Geert Vanden Bossche
Feb 08, 2026

We currently observe highly divergent trends in the viral evolutionary dynamics of BA.3.2 across distinct, highly Covid-19 (C-19)-vaccinated countries. I commented on this observation reported on X as follows:

https://x.com/GVDBossche/status/2020427259539071291

“BA.3.2 sublineages most likely reflect a metastable state under near-threshold immune pressure. Under such a scenario, heterogeneous and fluctuating detection rates across highly C-19-vaccinated countries are not only expected- they are totally consistent with a system approaching a qualitative evolutionary transition rather than endemic stabilization!”​

What the title of this article really means is that what appear to be different viral evolutionary ‘behaviors’ across countries are actually surface variations on the same underlying immune pressure and calling these behaviors ‘benign’ doesn’t make them stable or ‘endemic’!

If BA.3.2 variants are a sign that the virus is stuck in an unstable ‘in-between’ phase in highly C-19-vaccinated countries, then ups and downs in how often they are detected from one country to another are exactly what you would expect.

In this situation, the virus is not simply trying to become more contagious in a straightforward way.

Instead, it is struggling against widespread immunity that limits its ability to spread, making its success very sensitive to small differences between countries-such as vaccination (including boosting) rate and timing, how often people get reinfected, how much silent (asymptomatic) spread occurs or social behavior[1].

Because of this, even small changes can lead to noticeable rises or falls in BA.3.2 cases. The variant may appear to grow in one country, decline in another, and then reappear elsewhere without ever clearly taking over.

This back-and-forth pattern suggests the virus is ‘searching’ for a way out of a tight evolutionary corner, rather than settling into a calm, endemic state. In simple terms, these irregular fluctuations are a warning sign that the virus is under heavy pressure and approaching a critical turning point, not that it has stabilized or become harmless! (see previous Substack article: Lay summary on recent Substack article: "Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst...").


[1] This last factor is an extremely popular ‘scapegoat’ among public health authorities and so-called experts, mostly used inappropriately to explain whatever pandemic evolution, even when it follows a consistent course across different highly C-19 vaccinated populations.

 

[Heliobas Disciple]

View: https://www.youtube.com/watch?v=A41dhLfGzoI
Geert Says COVID Is Like A Pus Filled Abscess?
Vejon Health
Streamed live Feb 8, 2026
12 min 12 sec

In this video, I revisit Geert Vanden Bossche’s latest warning about where we are now in the COVID-19 trajectory. Unlike his 2021 focus on immune escape during mass vaccination, Geert’s current concern is that the virus has not been resolved but suppressed under sustained immune pressure — more like a pus-filled abscess than a healed infection. On the surface, transmission and severity may appear manageable, but underneath, viral evolution remains active, unstable, and constrained rather than settled into true endemic balance.

=======================================================
Lay summary on recent Substack article: "Everyone knows a pus-filled abscess will eventually burst. However, nothing is more difficult than predicting exactly when it will burst..."
https://voiceforscienceandsolidarity....
=======================================================

I explore what this analogy means biologically, how it relates to ongoing Omicron diversification, and why fluctuating variant patterns matter more than reassuring headlines suggest. This is not about predicting catastrophe or timelines, but about understanding risk: the difference between genuine resolution and contained instability. The key question is whether scientific leadership is once again mistaking temporary control for long-term safety — and whether ignoring uncomfortable signals now risks repeating the same error made earlier in the pandemic.

=======================================================

In this video, Dr. Philip McMillan discusses a recent Substack newsletter by Geert Vanden Bossche, focused on viral evolutionary behaviors and the complexities of predicting viral spread. This vital research explores the immune system's response in highly vaccinated countries and the emergence of new virus variants like BA.3.2. Understanding these dynamics is crucial for public health and science.

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/antihistamines-may-lower-long-covid-and-clot-risks

(fair use applies)


Antihistamines May Lower Long COVID and Clot Risks
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 03, 2026

A large new study from Spain is offering fresh hope that commonly used antihistamine medicines could play a meaningful role in reducing long COVID symptoms and dangerous blood clots after COVID-19 infection. The research focused on real world patient data and explored whether people already taking antihistamines had better long-term outcomes than those who were not.

Why Long COVID and Blood Clots Matter
Long COVID refers to symptoms that continue for months after the initial infection, including fatigue, brain fog, breathing problems, and heart issues. Blood clots are another serious concern, as COVID-19 has been linked to strokes, heart attacks, and lung clots, especially in older adults. This Medical News report highlights why researchers are urgently searching for simple and affordable ways to reduce these risks.

How The Study Was Conducted
Researchers analyzed anonymized health data from 192,651 people served by the Consorci Sanitari de Terrassa in the metropolitan area of Barcelona. The data covered March 2020 to March 2025 and included information on COVID-19 infections, vaccination status, long COVID diagnoses, blood clot events, age, gender, and long-term medication use. The team compared patients who were on chronic antihistamine treatment with those who were not.

Key Findings on Long COVID
Among people not taking antihistamines, long COVID became more common with each additional COVID-19 infection. In contrast, patients who were on long term antihistamines showed strikingly fewer cases. Notably, no long COVID cases were recorded in antihistamine users who had three documented COVID-19 infections. While some subgroups were small, the consistent pattern suggested a possible protective effect that deserves further investigation.

Strong Reduction in Blood Clot Events
The most robust finding involved blood clots. Between 2021 and 2024, clotting events increased steadily in the general population. However, people taking chronic antihistamines had far fewer clots. Only about 1.6 percent of antihistamine users experienced clots, compared to 3.3 percent of non-users with similar medical backgrounds. This difference remained significant even after adjusting for age, gender, vaccination, and other long-term treatments.

Why Antihistamines Might Help
Scientists believe antihistamines may reduce inflammation and block platelet activating factors that contribute to clot formation. Some antihistamines are already known to influence immune and vascular pathways, which could explain both the lower clot risk and the apparent reduction in long COVID symptoms.

Study Limitations and Caution
The researchers stressed that this was an observational study, not a randomized trial. Not all patients may have taken their medications consistently, and some cases may have gone undiagnosed. Still, the size of the population and the consistency of the findings make the results hard to ignore.

Conclusions
The findings suggest that long term antihistamine use is linked to fewer blood clots and possibly a lower risk of long COVID after COVID-19 infection. While antihistamines are not a cure and should not be self-prescribed for this purpose, the results strongly support launching controlled clinical trials. If confirmed, these widely available medicines could offer a low cost and accessible way to reduce serious long term COVID-19 complications.

Research Institutions
The researchers were from multiple primary care centers and institutions under the Consorci Sanitari de Terrassa, the Hospital Universitari de Terrassa, and the Faculty of Medicine at the Universitat de Barcelona in Spain.

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

https://www.mdpi.com/1999-4915/18/2/197

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/japan-s-covid-19-cases-surge-nearly-thirty-percent-as-hokkaido-emerges-as-a-hotspot

(fair use applies)


Japan’s COVID-19 Cases Surge Nearly Thirty Percent as Hokkaido Emerges as a Hotspot
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 03, 2026

Japan is once again seeing a notable rise in COVID-19 activity, with new data showing a sharp week-on-week increase that has caught the attention of health authorities and the public alike. During the reporting week of January 19 to January 25, national surveillance figures revealed a rise close to 30 percent compared to the previous week, signaling that the SARS-CoV-2 virus continues to circulate actively even in 2026.


Sharp Weekly Increase Raises Attention
According to Japan’s Ministry of Health, Labour and Welfare, the nationwide average number of COVID-19 patients per designated medical facility climbed to 1.99 for the January 19–25 period. This represented an increase of 0.45 patients per facility from the prior week, translating to an approximate 29 to 30 percent jump. This Medical News report highlights that the rise is based on Japan’s sentinel surveillance system, which tracks trends through fixed medical institutions rather than the mass testing approach used earlier in the pandemic.

In absolute terms, around 7,573 new infections were reported through sentinel clinics and hospitals for the week, reinforcing the view that transmission has accelerated across several regions.


Hokkaido Stands Out Among Prefectures
Regional data shows that Hokkaido emerged as the most affected prefecture during this period. The northern island recorded an average of 6.02 COVID-19 patients per medical facility, more than three times the national average. This places Hokkaido clearly at the top of the list, indicating a concentrated regional surge rather than a uniform nationwide spread.

Other northern and eastern prefectures also reported elevated figures. Yamagata posted an average of 5.10 patients per facility, while Tochigi followed closely at 5.89. In contrast, major urban centers such as Tokyo and Osaka reported significantly lower averages of 1.04 and 0.76 respectively, suggesting that the current wave is more pronounced in colder regions.


What The Surveillance Data Really Means
Health experts emphasize that sentinel surveillance is designed to detect trends rather than exact population-wide case numbers. A sustained rise in per-facility averages usually reflects increased community transmission, greater demand for outpatient care, and potential strain on local healthcare services, particularly if the trend persists for several weeks.

Seasonal factors are also believed to be playing a role. Colder weather, reduced ventilation indoors, and post-holiday social interactions can all contribute to increased viral spread during January and February.


Variant Responsible for the Surge Not Yet identified
According to local experts, the SARS-CoV-2 strains responsible for the surge have yet to be identified due to lack of genomic sequencing at many hospitals these days. However, many infected are exhibiting serious symptoms requiring them to be hospitalized.


Implications And Forward Outlook
The latest figures underscore that COVID-19 remains an active public health concern in Japan, even as it is managed alongside other respiratory infections. While authorities are not signaling broad restrictions, localized advisories and heightened vigilance in high-burden areas like Hokkaido are likely.

The key takeaway from the January 19–25 data is that the situation warrants close monitoring. A nearly 30 percent weekly rise, combined with strong regional clustering, suggests that healthcare systems and the public should remain cautious. Continued surveillance over the coming weeks will be critical to determine whether this surge stabilizes or evolves into a more sustained seasonal wave.


Reference

Coronavirus (COVID-19) infections in Japan - The Mainichi

Latest data on coronavirus (COVID-19) infections in Japan.

mainichi.jp

 

[Heliobas Disciple]

When Denying Viral Evolution Becomes a Substitute for Understanding It.

From Basic Virology, Immunology, Evolutionary Biology to Wishful Thinking: Why Some Arguments Collapse Under Data….

voiceforscienceandsolidarity.substack.com

(fair use applies)


When Denying Viral Evolution Becomes a Substitute for Understanding It.
From Basic Virology, Immunology, Evolutionary Biology to Wishful Thinking: Why Some Arguments Collapse Under Data….
Geert Vanden Bossche
Feb 09, 2026

I recently came across the following tweet from someone who clearly wanted to teach me some basic virology, immunology, and evolutionary biology, as she thought I desperately needed it. That person profoundly disagreed with a previous tweet reply of mine

Geert Vanden Bossche@GVDBossche​

@drtaubraun You claim this is ´not a conspiracy,´, yet immediately replace virology with a narrative of intentional depopulation, biological warfare and a virus that supposedly doesn’t mutate! That is not an alternative explanation - it is an abandonment of biology itself. My work does not​

3:10 PM · Feb 8, 2026 · 798 Views​

and reacted as follows:

… “However - I do take umbrage with some of the specific claims you make, such as “whoever rejects viral mutation, antigenic drift, recombination and selection is not disputing my theory - they are rejecting modern molecular biology outright.” I dispute your theory when it comes to that list of characteristics, because, on the whole, those unique behaviours are exclusive only to the Influenza virus. They are definitely not characteristics of coronavirus, or most other viruses for that matter. Antigenic drift, recombination and selection - happen with influenza because it lacks any proofreading ability. In contrast, Coronavirus does proofread and for that reason there is no antigenic drift or recombination - there never has been - and of course there is herd immunity. Humans are not the only mammals on earth Geert, so your theory that this virus is going to run out of options and us humans are going to cause immune pressure and force the virus to evolve or recombine - is probably false. Coronavirus spills over to another susceptible herd, so once it reaches the threshold limit, it disappears”​

Megan@MeganSuspended​

@GVDBossche @drtaubraun I agree with your overall response. Tau’s theory does abandoned basic science and cellular biology and in doing so, it just introduces another level of fault - not to mention confusion. The better approach, when determining the ‘truth’ would be for him to first falsify the status​

11:57 PM · Feb 8, 2026 ​

Here is what I replied:

“No matter how hard it is for me, I’ll try to stay calm. Although responding to comments built on such misconceptions is a poor use of time, I do so out of a sense of responsibility. Public discourse deserves protection from confidently delivered but scientifically illiterate claims that mislead readers under the guise of certainty based on alleged knowledge in the field. So, I hope your followers will read this too.​

​

Your objection rests on a cascade of fundamental misunderstandings about virology and viral evolution.​

​

First, antigenic drift, recombination, and selection are not exclusive to influenza. They are universal evolutionary mechanisms that apply to all replicating genetic systems, including coronaviruses (CoVs). While influenza lacks proofreading and therefore accumulates substitutions faster, SC-2 has demonstrated extensive antigenic drift in real time, documented by tons of sequenced genomes and thousands of peer-reviewed studies. Proofreading in viral replication means the polymerase corrects many copying errors, so the mutation rate becomes lower but not zero. Because some mutations still arise, natural selection continues to act on them, which allows viral antigenic evolution/ adaptation to proceed, just more slowly or constrained.​

​

Second, the claim that CoVs do not recombine is simply false. CoVs are, in fact, among the most recombinogenic RNA viruses known!! Recombination is typically associated with CoV evolution and has been repeatedly demonstrated for SC-2. This is not controversial; it is simply textbook virology!​

​

Third, your statement on herd immunity is totally contradicted by persistent (vaccine-breakthrough) reinfections, continuous variant turnover, immune escape and the absence of durable sterilizing immunity. Herd immunity requires stable transmission-blocking immunity, which none of the highly C-19-vaccinated populations has ever mounted against SC-2. Fourth, the suggestion that SC-2 can simply ‘escape’ immune pressure by spilling into other mammals reflects yet another misunderstanding of evolutionary constraints. Spillover does not reset viral adaptation!​

​

Cross-species transmission of co-circulating immune escape variants from highly C-19-vaccinated populations would impose high severe fitness costs and extremely challenging host-specific adaptation; furthermore, it does not relieve immune pressure in the population in which the virus replicates most frequently and in the largest numbers. For SC-2, that has overwhelmingly been the human population, especially highly C-19-vaccinated populations, where repeated vaccine breakthrough (re-)infections occur. Evolution follows replication density or selection pressure intensity-not the kind of wishful ecological shortcuts you’re proposing. Consequently, human immunity-not animal immunity-defines the dominant evolutionary immune pressure on SC-2!​

​

Fifth, the idea that SC-2 ‘runs out of options and disappears’ once a threshold is reached ignores basic evolutionary logic. When conventional mutational routes become constrained, selection favors qualitative shifts in phenotype, not extinction. This is precisely what my analysis addresses.​

​

Last but not least, your attempt to dismiss viral mutation, drift, recombination and selection occurring during this ‘immune escape’ pandemic does not challenge my theory-it rejects modern molecular biology outright and constitutes a ridiculous denial of empirical reality.”​

​

​

 

[Heliobas Disciple]

No PH authority should intervene in a pandemic without understanding the mechanisms underlying the viral evolutionary dynamics, just as no MD should treat a sick patient without an accurate diagnosis

The question that no public health (PH) authority seems able to resolve is whether the currently observed viral evolutionary dynamics are best explained by ‘endemic coexistence’ of currently co-circulating SARS-CoV-2 (SC-2) immune-escape variants or by ‘

voiceforscienceandsolidarity.substack.com

(fair use applies)


No PH authority should intervene in a pandemic without understanding the mechanisms underlying the viral evolutionary dynamics, just as no MD should treat a sick patient without an accurate diagnosis
Geert Vanden Bossche
Feb 09, 2026

The question that no public health (PH) authority seems able to resolve is whether the currently observed viral evolutionary dynamics are best explained by ‘endemic coexistence’ of currently co-circulating SARS-CoV-2 (SC-2) immune-escape variants or by ‘evolutionary exhaustion’ of SC-2 under immune pressure. Yet this is clearly the defining and most pressing evolutionary question at present!

Let’s analyze the competing arguments logically, mechanistically, and probabilistically.


The Competing Hypotheses

—> Mainstream view: SC-2 evolves toward endemic coexistence

Some people-often referred to (disapprovingly or not!) as ‘experts’-propose that BA.3.2 marks a phase shift from serial replacement (sweeps) to concurrent co-circulation (equilibrium).

Their reasoning is as follows:

For the first time, one variant (BA.3.2) is not sweeping away others. Epidemiological data from several countries show ‘stabilization’ rather than exponential growth. Hence, the viral ecosystem may be entering a multi-clade equilibrium, similar to seasonal influenza or common cold coronaviruses.

If this were true, human populations would have reached a broad immunological homeostasis with sufficient background immunity to prevent any single lineage from dominating globally. This is why, at least in their view, the virus persists but stabilizes at low to moderate, manageable transmission rates.
That sounds rather optimistic, although simplistic, and it typically reflects the position adopted by the vast majority of PH authorities and so-called ‘experts.’

—> Geert Vanden Bossche’s view: BA.3.2-derived (sub)lineages experience serious immune escape constraints and a phase transition to higher virulence is impending, threatening highly COVID-19(C-19)-vaccinated populations.

I assert that evolutionary stagnation can be deceptive: BA.3.2’s behavior is not an indication of true equilibrium but of evolutionary exhaustion under relentless vaccine-induced immune pressure.

Why?

i) The spike (S) protein has accumulated ~50 mutations yet shows no substantial gain in transmissibility.

ii) Persistent minor growth signals, associated with a lack of dominance, indicate evolutionary stagnation under constraint.

iii) True endemic equilibrium would not require such mutational ‘effort’ to maintain population-level presence.

The current plateau therefore marks a metastable state-i.e., a system running out of conventional options that may soon undergo a nonlinear shift (e.g., novel entry pathways [ACE2-independent!], tropism changes, recombination and additional glycosylation).

This is fundamentally a thermodynamic interpretation:
the virus is approaching the boundary of accessible mutational space, constrained by immune pressure.

But let’s examine what the biology supports in terms of:

1. Immune landscape

The world’s population is now largely ‘immune-imprinted.’ Most people received vaccines with similar S antigens and have been (re-)infected with Omicron-like lineages or otherwise boosted by additional (updated) vaccine doses.

This shared imprint narrows the evolutionary corridor available to the virus.

Under such constraint, new variants do not compete via raw transmissibility but via immunological niche differentiation, i.e., they employ subtle evasion tactics (e.g., glycan shifts or unusual amino acid mutations requiring conformational compensatory changes to yield marginal increases in receptor binding or resistance to neutralization).
This is classic constrained evolution, not the establishment of stable equilibrium!

2. Mutation load

A variant accumulating >50 S mutations with only marginal advantage indicates heavy compensatory mutation: the virus mutates not just to improve function but to recover losses caused by other mutations. Such a ‘fitness plateau’ is well-documented in evolutionary biology; it is a red flag for exhaustion, not successful adaptation!

3. Epidemiology

Slow or stagnant expansion (as with BA.3.2) matches a system where immune pressure and adaptive capacity are in temporary balance-a dynamic equilibrium doomed to shift. Hence, while it may appear as stable and peaceful co-circulation of SC-2 immune-escape variants (‘endemic coexistence’), from a systems perspective it is more likely a tensioned equilibrium, i.e., metastable rather than stable.


Hypothesis Comparison: Degree of Support and Likelihood

In contrast to the ‘endemic coexistence’ hypothesis, my ‘pre-transition’ hypothesis is strongly supported by BA.3.2’s high mutation load with marginal return, the convergent evolution of newly emerging co-circulating lineages and the high but suboptimal immune pressure exerted by highly C-19-vaccinated populations.

If my theory is correct, one would expect minor periodic immune ‘resets’ to continue for some more time, thereby maintaining the virus in circulation. However, this would not occur without increasing the risk of an explosive emergence of a new type of coronavirus with qualitatively altered pathogenic behavior, using novel entry pathways (ACE2-independent!) and thereby shifting SC-2’s tropism from the upper respiratory tract toward the blood and distant organs (Plausibility of more extended O-glycosylation as last resort for SARS-CoV-2 immune escape).

As my theory considers the current stagnation of BA.3.2 to be a metastable phenomenon, it is reasonable to assume that it implies escape variant diversity collapsing suddenly, not through elimination but through an abrupt phase transition.

It goes without saying that in such a scenario, continued boosting campaigns with homologous antigens, as recommended by public health authorities and ‘experts’, will only accelerate this explosion by enhancing selective immune pressure on viral transmissibility and freezing immune diversity.

Bottom Line

Even though-precisely because of the potentially catastrophic implications—I am trying as hard as I can to subject my hypothesis to maximum scrutiny and criticism, I still cannot conceptually disprove it at this point. I believe its strength comes from drawing on multiple disciplines and seamlessly integrating virology, immunology, vaccinology and evolutionary biology.

It perfectly explains why BA.3.2 is so mutationally saturated yet not dominating and even why its prevalence fluctuates across different countries
(Lay Summary on: "Same feed, different fleas: why BA.3.2 looks different across highly Covid-19-vaccinated countries without being benign!").

It aligns with real-world evolutionary bottlenecks observed in influenza after excessive antigenic drift whereas, on the other hand, the mainstream hypothesis of ‘benign endemic coexistence’ could only hold if immune selection pressures had truly relaxed; however, large-scale C-19 vaccination combined with recurring vaccine-breakthrough infections in highly C-19 vaccinated populations ensures the exact opposite.

 

[Heliobas Disciple]

https://scitechdaily.com/scientists-find-new-immune-clue-behind-long-covids-lingering-symptoms/

(fair use applies)


Scientists Find New Immune Clue Behind Long COVID’s Lingering Symptoms
By Helmholtz Centre for Infection Research
February 4, 2026

A detailed analysis of immune cells in Long COVID patients has revealed a previously unknown molecular signature linked to lingering symptoms.

In Germany, Long COVID develops in up to about one in ten people after an infection with the SARS-CoV-2 virus. For some, the illness does not end when the virus clears. Instead, a mix of problems can linger, ranging from crushing fatigue and “brain fog” to breathing difficulties and neurological symptoms. The experience is not the same for everyone, which has made Long COVID especially challenging to pin down.

“Long COVID is an extremely complex disease with various manifestations,” says Prof. Yang Li, head of the “Computational Biology for Individualised Medicine” department and director of CiiM. “How and to what extent Long COVID develops is still largely unknown. Figuratively speaking, we are unfortunately only looking at an extremely incomplete puzzle.”

A major reason that puzzle remains incomplete is that Long COVID is likely not a single condition with one cause. Researchers increasingly suspect it can arise through multiple biological pathways, such as lingering inflammation, immune misfiring, or subtle tissue stress that persists long after the initial infection.

To find clearer signals amid that complexity, Yang Li and colleagues partnered with teams led by Prof. Thomas Illig (MHH) and Prof. Jie Sun (University of Virginia, USA), as well as other collaborators, to search for measurable immune patterns that might help explain why symptoms persist.
Searching for Molecular Clues

Instead of relying only on broad blood tests, the researchers zoomed in on individual immune cells from Long COVID patients, using samples drawn from MHH’s central biobank. Looking at single cells matters because immune responses can be patchy. Two people can have similar symptoms while very different immune cell populations are driving them.

“We examined the cells using a so-called single-cell multiomics approach. This allowed us to record the molecules’ status within a cell and gain insights into its cellular relationships,” explains Dr Saumya Kumar, CiiM scientist and first author of the study.

In practical terms, this approach let the team map immune cell “states” in fine detail. That kind of resolution can reveal whether certain cells are acting unusually, even if the overall immune system looks only mildly altered when averaged across millions of cells.

The researchers also measured levels of pro-inflammatory signaling molecules known as cytokines in blood plasma. Cytokines act like biological alerts, helping immune cells communicate and coordinate responses. When those signals stay elevated, they can hint at ongoing inflammation that may track with persistent symptoms.

“The central and innovative approach of our study is to classify patient data according to the severity of the original COVID-19 disease,” says Yang Li. “This approach allowed us to capture the associated molecular differences in immune response across patients. Only in this way, clear molecular characteristics underlying the chronic symptoms of Long COVID could be identified.”


Immune Cell Changes Over Time

The study tackled questions that matter to patients and clinicians alike: Do immune cells settle into recognizable patterns during Long COVID? Are there molecular fingerprints that align with how severe fatigue feels, or how hard it is to breathe?

By applying big-data analysis across the single-cell results, the researchers homed in on a specific immune cell population: CD14+ monocytes. These cells are part of the body’s first-line immune defense, patrolling the bloodstream and helping coordinate inflammatory responses. They are also known for their ability to shift gears quickly, which makes them useful for fighting infections but also a potential trouble spot if inflammation fails to switch off.
Links to Symptoms and Inflammation

“With the help of single-cell analysis, we were able to zoom in on these cells. This revealed that monocytes with a specific molecular state (i.e. molecular profile), which we called “LC-Mo”, were particularly prevalent in Long COVID patients who had previously experienced mild to moderate COVID-19 disease,” says Saumya Kumar. “In addition, LC-Mo correlated with the severity of fatigue and respiratory symptoms and was associated with elevated cytokine levels in blood plasma, which are an indicator of inflammatory processes in the body.”

With LC-Mo, the researchers have thus found an important new piece of the puzzle. “Its exact place in the pathogenesis of Long COVID has yet to be determined, but it offers exciting starting points for further studies, for example, with regard to genetic risk factors or individualised medicine,” says Yang Li. “If we can gain a better understanding of the background to the development of Long COVID, it will also help us to better understand the development of possible late or long-term consequences of other infectious diseases.”

Reference: “A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID” by Saumya Kumar, Chaofan Li, Liang Zhou, Qiuyao Zhan, Ahmed Alaswad, Sonja Volland, Bibiana Costa, Simon Alexander Krooss, Isabel Klefenz, Hagen Schmaus, Antonia Zeuzem, Dorothee von Witzendorff, Helena Lickei, Lea Pueschel, Anke R. M. Kraft, Markus Cornberg, Andreas Rembert Koczulla, Isabell Pink, Marius M. Hoeper, Cheng-Jian Xu, Susanne Häussler, Miriam Wiestler, Mihai G. Netea, Thomas Illig, Jie Sun and Yang Li, 14 January 2026, Nature Immunology.
DOI: 10.1038/s41590-025-02387-1

The research was funded by an ERC Starting Grant (ModVaccine), the COVID-19 Research Network of Lower Saxony (COFONI) and the Lower Saxony Centre for AI & Causal Methods in Medicine (CAIMed), both with funds from the Lower Saxony Ministry of Science and Culture (MWK), as well as the Federal Ministry of Research, Technology and Space (BMFTR).

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/vitamin-d-shows-hope-against-post-covid-fatigue-syndrome

(fair use applies)


Vitamin D Shows Hope Against Post-COVID Fatigue Syndrome
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 06, 2026


Medical News: Vitamin D Deficiency and Lingering Post Covid Illness
A new clinical study from Japan is offering renewed hope to people suffering from long lasting fatigue and multiple unexplained symptoms after COVID-19 infection or vaccination. Many patients develop a condition known as myalgic encephalomyelitis or chronic fatigue syndrome, marked by extreme tiredness, brain fog, sleep disturbances, pain, dizziness, and worsening symptoms after physical or mental effort. Researchers suspected that low vitamin D levels might be playing a critical role in worsening or prolonging these symptoms.


Why Researchers Focused on Vitamin D
Vitamin D is known to influence immune balance, inflammation control, and nerve health. Earlier observations showed that many patients who developed chronic fatigue after COVID-19 vaccination or infection had insufficient or deficient vitamin D levels. This Medical News report explores whether correcting that deficiency could meaningfully improve daily functioning and reduce symptom burden.


How The Study Was Conducted
The randomized controlled trial involved 91 adults diagnosed with chronic fatigue syndrome following either COVID-19 infection or vaccination. All participants had low blood levels of vitamin D. The study was conducted across five medical centers in Japan. Participants were divided into two groups. One group received standard active vitamin D medication alone. The other group received the same medication plus structured vitamin D replacement guidance, including daily vitamin D supplementation, dietary advice, sunlight exposure, and light exercise.


Clear And Measurable Improvements Seen
After 12 weeks, patients receiving the full vitamin D replacement guidance showed striking improvements. On average, they experienced a reduction of nearly seven symptoms, compared to just over one symptom in the control group. Blood vitamin D levels rose significantly in the guided group, while levels in the control group barely changed. Importantly, 16 patients in the guided group improved enough that they no longer met diagnostic criteria for chronic fatigue syndrome, compared to only one patient in the control group.


Benefits Seen in Both Long COVID and Post Vaccine Cases
The improvements were consistent whether symptoms followed COVID-19 infection or vaccination. Patients reported better sleep, reduced pain, improved immune related symptoms, and less post exertional exhaustion. Safety monitoring showed no serious vitamin D related side effects, and laboratory values remained stable.


What These Findings Mean for Patients
The results suggest that simple and affordable vitamin D correction strategies may offer meaningful relief for people struggling with long term post COVID fatigue conditions. The study also highlights that active vitamin D medication alone may not be sufficient to correct deficiency or improve symptoms without proper supplementation and lifestyle guidance.


Conclusion
This study provides strong clinical evidence that addressing vitamin D deficiency can significantly reduce symptom severity in chronic fatigue syndrome linked to COVID-19 infection or vaccination. While vitamin D is not a cure, restoring healthy levels appears to support immune balance, reduce inflammation, and improve overall symptom burden, offering a practical therapeutic option for a condition with limited existing treatments.

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

https://www.mdpi.com/2072-6643/18/3/521

 

[Heliobas Disciple]

https://scitechdaily.com/a-tiny-antibody-just-crushed-the-coronaviruss-secret-weak-spot/

(fair use applies)


A Tiny Antibody Just Crushed the Coronavirus’s Secret Weak Spot
By Vlaams Instituut voor Biotechnologie
February 5, 2026

Researchers have identified a special type of small antibody that offers strong protection against a wide variety of SARS-related coronaviruses. These include the original SARS-CoV-1 as well as multiple versions of SARS-CoV-2, the virus that causes COVID-19. The antibodies work by attaching to a highly conserved and essential region located at the base of the virus’s spike protein. This action prevents the spike from changing shape, which is necessary for the virus to infect cells. The study, published in Nature Communications, could help pave the way for broad antiviral treatments that stay effective even as new variants emerge.


Why New Variants Make Antibody Treatments Less Effective

As SARS-CoV-2 continues to evolve, it produces new variants that can evade many existing antibody therapies. This is because most antibodies are designed to target regions of the spike protein that frequently mutate, like the receptor binding domain. When these regions change, antibodies may no longer recognize the virus, making treatments less effective or even useless.

To get around this problem, scientists led by Professor Xavier Saelens and Dr. Bert Schepens at the VIB-UGent Center for Medical Biotechnology decided to focus on a different part of the spike protein. They targeted the S2 subunit, which plays a key role in helping the virus fuse with human cells. Unlike other parts of the spike protein, the S2 subunit is much more stable across different types of coronaviruses.


Llama Antibodies Provide a Powerful New Tool

To find the right kind of antibodies, the team turned to llamas—specifically, one named Winter. Llamas produce single-domain antibodies (also known as VHHs or nanobodies) that are much smaller than typical human antibodies. The researchers discovered several of these llama-derived nanobodies that could neutralize a broad range of SARS-related viruses.

What sets these antibodies apart is how they work. Instead of targeting the virus’s usual weak spots, they act like a clamp. They attach to a rarely exposed, tightly conserved region made up of three twisted protein structures (called a coiled coil of alpha helices) at the base of the spike protein. By binding to this region, the antibodies lock the spike in its original shape and block it from unfolding—an essential step in the infection process.


Strong Protection, Even When the Virus Tries to Fight Back

In lab tests, these antibodies provided strong protection against infection in animals, even when given in small amounts. When researchers tried to force the virus to evolve and escape the treatment, it had a hard time doing so. The few variants that did emerge were much less infectious, suggesting that the virus cannot easily mutate this region without losing its ability to spread effectively.

“This region is so crucial to the virus that it can’t easily mutate without weakening the virus itself,” said Dr. Schepens, the study’s senior author. “That gives us a rare advantage: a target that’s both essential and stable across variants.”


Hope for Long-Lasting COVID and Coronavirus Treatments

This discovery marks an important step toward developing long-lasting antiviral therapies that could remain effective against current and future coronavirus threats.

“The combination of high potency, broad activity against numerous viral variants, and a high barrier to resistance is incredibly promising,” said Prof. Saelens. “This work provides a strong foundation for developing next-generation antibodies that could be vital in combating not only current but also future coronavirus threats.”

Reference: “Ultrapotent SARS coronavirus-neutralizing single-domain antibodies that clamp the spike at its base” by Sieglinde De Cae, Inge Van Molle, Loes van Schie, Sophie R. Shoemaker, Julie Deckers, Nincy Debeuf, Sahine Lameire, Wim Nerinckx, Kenny Roose, Daria Fijalkowska, Simon Devos, Anne-Sophie De Smet, Jackeline Cecilia Zavala Marchan, Toon Venneman, Koen Sedeyn, Lejla Mujanovic, Marlies Ballegeer, Manon Vanheerswynghels, Caroline De Wolf, Hans Demol, Jasper Zuallaert, Pieter Vanhaverbeke, Gholamreza Hassanzadeh Ghassabeh, Chiara Lonigro, Viki Bockstal, Manuela Rinaldi, Rana Abdelnabi, Johan Neyts, Susan Marqusee, Bart N. Lambrecht, Nico Callewaert, Han Remaut, Xavier Saelens and Bert Schepens, 30 May 2025, Nature Communications.
DOI: 10.1038/s41467-025-60250-1

Funding: Fonds Wetenschappelijk Onderzoek, EOS-programme, EU Horizon 2021, Exevir Bio BV

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/how-sugars-on-human-cells-help-covid-19-virus-spread

(fair use applies)


How Sugars on Human Cells Help COVID-19 Virus Spread
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 07, 2026

Medical News: A Hidden Sugar Based Pathway That Helps the Virus Attach and Infect
Scientists are continuing to uncover surprising details about how the SARS-CoV-2 virus infects human cells. While most people are familiar with the virus binding to the ACE2 receptor, new research shows that complex sugars on human cells also play a crucial role in helping the virus attach, linger, and spread more efficiently. This Medical News report highlights findings from a comprehensive review that explains these mechanisms in a clear and accessible way.


Understanding Glycans and Lectins in Simple Terms
Glycans are sugar chains found on the surface of nearly all human cells. Lectins are proteins that can recognize and bind to these sugars. Together, they form a communication system that cells use for many normal functions. However, viruses have learned to exploit this system. The review explains that SARS-CoV-2 uses these sugar structures as temporary docking points before firmly attaching to ACE2 receptors, increasing the chances of successful infection.


How The Virus Uses Sugar Coatings to Its Advantage
The SARS-CoV-2 spike protein is covered with dozens of sugar molecules. These sugars do more than hide the virus from the immune system. The study explains that certain sugars help stabilize the spike protein in a shape that makes it easier to bind to human cells. Some of these sugar structures also interact with lectins on immune cells, allowing the virus to hitch a ride and spread within the body without immediately infecting those immune cells.


Blood Groups and Infection Risk
One of the most striking findings discussed in the review involves blood groups. The researchers explain that the virus shows a preference for binding to sugar structures associated with blood group A, which are commonly found on the lining of the respiratory tract. This may help explain why people with blood group A have been observed to have a slightly higher risk of infection, while blood group O appears to offer some protection due to the absence of these sugar markers.


Similar Tricks Used by Other Viruses
The review compares SARS-CoV-2 to viruses like influenza, HIV, and norovirus. Many of these pathogens also rely on sugar-based attachment strategies. Influenza binds to sialic acid sugars, while norovirus depends heavily on blood group sugars. This comparison shows that exploiting glycans is a common and evolutionarily successful viral strategy.


Why These Findings Matter
Understanding these sugar-based interactions opens new doors for treatments. The study suggests that drugs or therapies designed to block these glycan or lectin interactions could reduce viral attachment and slow infection. Such approaches may work alongside vaccines and antiviral drugs to offer broader protection.


Conclusion
This revie w makes it clear that SARS-CoV-2 infection is not driven by a single receptor alone. Instead, the virus uses a complex network of sugar molecules and binding proteins to improve its chances of survival and spread. By uncovering these hidden interactions, scientists are gaining valuable insights that could shape future antiviral strategies and better prepare the world for emerging viral threats.


Institutions of the Researchers:
Department of Biochemistry and Convergence Medical Science, Institute of Medical Science, College of Medicine, Gyeongsang National University, Jinju, Republic of Korea.

The study findings were published in the peer reviewed International Journal of Molecular Sciences

https://www.mdpi.com/1422-0067/27/3/1608

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/covid-19-infection-linked-to-sudden-crohn-s-disease-onset

(fair use applies)


COVID-19 Infection Linked to Sudden Crohn’s Disease Onset
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 07, 2026

Medical News: A newly published case study from Japan is drawing fresh attention to how COVID-19 may trigger serious long term gut disorders, even in young and previously healthy individuals. Researchers report that a teenage patient developed Crohn’s disease only weeks after a SARS-CoV-2 infection, raising concerns that lingering digestive symptoms after COVID-19 should not be casually dismissed.

COVID-19 and the Gut a Troubling Connection
While COVID-19 is best known for affecting the lungs, doctors have long observed that the virus can also attack the digestive system. Diarrhea, abdominal pain, and nausea are now recognized as common symptoms during and after infection. However, what makes this case unusual is that the gastrointestinal symptoms never fully resolved and instead progressed into a chronic inflammatory bowel disease.

According to this Medical News report, an 18-year-old male developed persistent watery diarrhea, abdominal pain, low grade fever, and significant weight loss after testing positive for COVID-19. Despite recovering from the viral infection itself, his digestive symptoms continued for two months, prompting further medical investigation.

Advanced Testing Reveals Crohn’s Disease
Doctors performed detailed blood tests, imaging scans, and an ileocolonoscopy to identify the cause of his ongoing illness. Results showed severe inflammation of the small intestine and colon, along with classic Crohn’s disease features such as longitudinal ulcers and a cobblestone appearance of the intestinal lining. Fecal calprotectin levels, a marker of intestinal inflammation, were extremely elevated, confirming active disease.

Biopsy samples ruled out infections and other conditions, leading physicians to a firm diagnosis of moderately active Crohn’s disease involving both the ileum and colon.

Treatment Brings Relief and Remission
The patient was treated with corticosteroids to rapidly control inflammation, followed by long term immune suppressing medication to maintain remission. His symptoms improved quickly, and after one year of follow up, he remains stable with no disease flare ups. This outcome highlights the importance of early diagnosis and timely treatment.

Why COVID-19 May Trigger Crohn’s Disease
Researchers believe SARS-CoV-2 can infect intestinal cells directly by binding to ACE2 receptors in the gut. This may disrupt the intestinal barrier, alter gut bacteria, and overstimulate immune responses in genetically susceptible individuals. Such immune dysregulation may act as a trigger for Crohn’s disease rather than merely causing temporary post viral diarrhea.

Why This Case Matters
Although rare, similar cases have now been reported worldwide, suggesting a possible link between COVID-19 and ne w onset inflammatory bowel disease. Clinicians are urged to investigate persistent diarrhea after COVID-19 rather than attributing it solely to long COVID.

Conclusion
This case reinforces the need for heightened clinical awareness when gastrointestinal symptoms persist after COVID-19 infection. Prolonged diarrhea, weight loss, fever, or elevated inflammatory markers should prompt thorough evaluation, including colonoscopy when appropriate. Early recognition of Crohn’s disease can prevent long term bowel damage, improve quality of life, and ensure patients receive effective treatment before complications arise.

The study was conducted by researchers from the Department of General Medicine, Department of Gastroenterology and Hepatology, and the Division of Pathology at the Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan.

The study findings were published in the peer reviewed journal: Case Reports in Gastrointestinal Medicine.

https://onlinelibrary.wiley.com/doi/10.1155/crgm/2252518

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/covid-19-immune-damage-quietly-fuel-cancer-risks

(fair use applies)


COVID-19 Immune Damage Quietly Fuel Cancer Risks
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 08, 2026

A new scientific review is raising fresh concerns about how COVID-19 may leave behind long-lasting immune damage that could quietly increase cancer risks in some people. Researchers from the Institute of Microbiology and Virology at Riga Stradins University in Latvia examined growing evidence that SARS-CoV-2 infection can disrupt immune balance in ways that resemble mechanisms already known to support cancer development. This Medical News report highlights why scientists say long-term monitoring of COVID-19 survivors may be essential.

How COVID-19 Disrupts the Immune System
When SARS-CoV-2 enters the body, the immune system usually launches a strong attack to eliminate it. In many people, this response resolves normally. However, the researchers explain that a significant subset of patients develop lingering immune disturbances marked by chronic inflammation, exhausted immune cells, and poor tissue repair. These immune changes are now widely associated with long COVID and may persist for months or even years after infection.

Chronic Inflammation and Cancer Pathways
The review outlines how persistent inflammation after COVID-19 mirrors biological processes that drive cancer. Constant release of inflammatory chemicals such as interleukin-6 and tumor necrosis factor can damage DNA, promote abnormal cell growth, and weaken the immune system’s ability to detect early cancer cells. The authors note that these same pathways are well-known contributors to tumor formation and progression.

Viral Proteins and Cellular Stress
Beyond whole-virus infection, individual SARS-CoV-2 proteins may also interfere with normal cell signaling. The spike and membrane proteins have been shown in laboratory studies to activate molecular pathways linked to cell survival, scarring, and uncontrolled growth. These pathways, including NF-?B and JAK-STAT signaling, are frequently overactive in cancers and may create an environment that allows damaged cells to thrive.

Immune Exhaustion and Reduced Surveillance
Another key concern discussed in the study is immune exhaustion. After COVID-19, some patients show reduced numbers of effective T-cells and natural killer cells, which are crucial for destroying infected or abnormal cells. This weakened immune surveillance may reduce the body’s ability to eliminate emerging cancer cells, especially in individuals with prolonged symptoms or pre-existing health conditions.

What This Means Going Forward
In conclusion, the review emphasizes that SARS-CoV-2 is not classified as a cancer-causing virus, but its long-term effects on the immune system may indirectly influence cancer risk in vulnerable individuals. The authors call for careful long-term follow-up of COVID-19 survivors, particularly those with long COVID, to better understand immune recovery, cancer surve illance needs, and preventive strategies.

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

https://www.preprints.org/manuscript/202602.0176

 

[Heliobas Disciple]

https://www.thailandmedical.news/news/glutathione-emerges-as-key-defender-against-covid-19-and-tb

(fair use applies)


Glutathione Emerges as Key Defender Against COVID-19 And TB
Nikhil Prasad Fact checked by:Thailand Medical News Team
Feb 08, 2026

Scientists uncover how a natural antioxidant shapes immune strength in two global diseases
Researchers are increasingly turning their attention to glutathione, a naturally occurring antioxidant in the human body, after new scientific insights revealed its critical role in regulating immune defenses against both COVID-19 and tuberculosis (TB). These two diseases, although caused by very different pathogens, share striking similarities in how they overwhelm the immune system, especially in people already burdened by chronic illnesses or metabolic disorders. This Medical News report highlights how glutathione may represent a common biological thread linking severe disease outcomes.

Why COVID-19 and Tuberculosis Share Hidden Weaknesses
COVID-19 and tuberculosis remain major global health threats, particularly among older adults, people with diabetes, obesity, and chronic inflammation, and those with limited access to healthcare. Scientists note that in both illnesses, severe disease is often driven less by the pathogen itself and more by immune dysfunction, excessive inflammation, and oxidative stress. Oxidative stress occurs when harmful molecules overwhelm the body’s natural defenses, damaging cells and tissues. Glutathione acts as the body’s main internal shield against this process.

Glutathione’s Role in Immune Balance
Glutathione helps immune cells function properly by maintaining redox balance, a delicate chemical state that allows immune signaling without triggering harmful inflammation. The study explains that low glutathione levels can impair the ability of immune cells such as macrophages and T cells to fight infections effectively. In tuberculosis, this deficiency weakens the body’s ability to contain bacteria within protective structures known as granulomas. In COVID-19, depleted glutathione is linked to uncontrolled cytokine release, vascular damage, and blood clot formation.

Why High-Risk Populations Are More Vulnerable
Many of the strongest risk factors for severe COVID-19 and tuberculosis, including aging, diabetes, and cardiovascular disease, are also associated with naturally lower glutathione levels. This means these individuals start infections with a reduced capacity to manage oxidative stress. When infection strikes, their immune systems are more likely to spiral into damaging inflammation rather than mount a controlled defense.

Potential For Host-Focused Strategies
Instead of targeting pathogens alone, scientists are increasingly interested in host-directed strategies that strengthen the body’s resilience. The findings suggest glutathione could be a valuable focus of future research as a modifiable host factor. While the researchers caution that glutathione is not a cure or guaranteed preventive measure, they emphasize that improving redox balance could support healthier immune responses in vulnerable populations.

Institutions Behind the Research
The study was conducted by researchers from the College of Osteopathic Medicine of the Pacific at Western University of Health Sciences in Pomona, California, and the Department of Biochemistry and Chemistry at the University of California, Los Angeles.

Conclusion
Overall, the findings present glutathione as a central regulator of immune resilience rather than a simple antioxidant. By influencing inflammation, immune coordination, and tissue protection, glutathione may help explain why some individuals develop severe COVID-19 or tuberculosis while others recover more easily. These insights strengthen the case for further investigation into host-focused approaches that complement existing treatments and public health strategies.

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

https://www.mdpi.com/2076-3921/15/2/214

 

[Profit of Doom]

I wonder what vitamin D dosage that study was using, and what levels they achieved. I take 15,000 IU plus K2. Showing around 50 test results.