A large real-world preprint analysis (~193,000 people, 2020–2025) suggests that people chronically taking antihistamines had
fewer thrombotic events
and almost no recorded long COVID - even after multiple reinfections.
This is not proof. But it is not noise either.
First, the basics.
This is an observational study, not a randomized trial.
So it cannot establish causality.
What it can do is identify patterns worth taking seriously - especially when they are consistent across subgroups.
What stood out most strongly?
Thrombosis
Among people with at least one chronic medication
antihistamine users ~1.6%
non-users ~3.3%
The difference was statistically robust and persisted across age, sex, vaccination status, and infection history.
This is the strongest signal in the dataset.
Long COVID
In people not using antihistamines, long COVID prevalence increased with each reinfection - especially after the third.
In the antihistamine group
no recorded long COVID cases after 2 or ≥3 infections
Numbers are smaller here, so caution is required - but the pattern is striking.
Naturally, the next question is
Do we have RCTs for this?
Short answer. No - not for prevention.
So how should this be interpreted?
Not as a miracle cure.
But as a biologically plausible signal -
histamine pathways affect neuroinflammation
antihistamines can modulate platelet-activating factor (PAF)
PAF is linked to microthrombosis and vascular inflammation
This fits existing biology.
The uncomfortable reality - antihistamines are cheap, generic, off-patent.
Which means large preventive RCTs are unlikely without public funding.
Absence of RCT evidence here reflects lack of incentives, not lack of relevance.
This preprint does not prove anything -
but it raises a clear, coherent, and testable hypothesis.
Ignoring such signals is not scientific caution.
It is scientific inertia.
Immunity that once protected us from deadly infections
may now increase the risk of autoimmunity, Long COVID, and chronic inflammation.
A new review explains whyđź§µ
Here’s the paradox.
The strongest genetic risk factors for autoimmune diseases are also some of the oldest immune genes we carry.
If they were purely harmful, evolution would have removed them long ago.
A review in Frontiers in Immunology focuses on a small group of ancestral HLA class II haplotypes -
DR2-DQ6, DR3-DQ2, and DR4-DQ8 - and their role in this paradox.
COVID-19 is often described as an inflammatory disease.
But new research shows SARS-CoV-2 goes deeper.
It alters regulatory layers inside cells at the RNA level, weakening antiviral defense from within.đź§µ
Thanks @NFMai @RWittenbrink
Cells contain long non-coding RNAs (lncRNAs).
They don’t make proteins - they act as control hubs, coordinating immune signals, especially interferon (IFN) responses.
RNA function isn’t fixed.
It can be fine tuned by a chemical mark called m6A methylation, which changes RNA shape, interactions, and behavior - without changing RNA levels.
Severe COVID-19 leaves behind a long-lasting, systemic, and biologically measurable pro-oncogenic state
that persists for at least one year after infection and may increase cancer risk or worsen cancer prognosisđź§µ
The authors analyzed long-term changes in gene expression in peripheral blood mononuclear cells (PBMCs) one year after COVID-19 infection.
They focused on differences between mild disease and severe COVID-19 with pneumonia, and on how these long-lasting changes relate to biological pathways involved in cancer.
COVID-19 is not just an acute event - it is a long-term vascular insult.
This study shows that the risk of ischemic stroke remains elevated for at least four years after SARS-CoV-2 infection.đź§µ
The risk remains elevated including in people who
were not hospitalized,
had a mild or moderate course,
had no obvious neurological complications during the acute phase.
This strongly suggests that SARS-CoV-2 is consistent with lasting structural or functional vascular injury to the vascular system, rather than causing only a transient pro thrombotic episode.
What a new Nature Immunology study shows about long COVID?
Long COVID is not post-infectious fatigue.
A new study shows that it is a clearly defined biological state =
chronic immune activation, T-cell exhaustion, and metabolic disruptionđź§µ
The study analyzed 142 individuals, including 28 patients with long COVID.
Compared with recovered controls, people with long COVID showed persistent activation of inflammatory pathways lasting more than 180 days after infection.
These pathways include IL-6, IFN-γ, JAK–STAT signaling, complement activation, and coagulation pathways.
This pattern does not look like recovery.
It looks like an immune system that remains stuck in an activated state.
Can pathological processes continue in the brain without an active virus?
Yes.
The SARS-CoV-2 nucleocapsid (N) protein on its own can accelerate microglial aging by switching cellular metabolism toward glycolysis, leading to measurable memory impairmentđź§µ
This study shows that the N protein is not biologically neutral.
Even in the absence of viral replication, it is sufficient to trigger long-lasting dysfunction in the brain.
What exactly is being damaged?
The primary target is microglia, the brain’s immune cells.
They are not merely activated.
They are metabolically reprogrammed.