Zdenek Vrozina Profile picture
Jun 19 12 tweets 3 min read Read on X
A major new review from Yale (Moen, Baker, Iwasaki, 2025) offers the most comprehensive picture yet of what SARS-CoV-2 does to the nervous system.
The conclusion is stark:
Long COVID is a chronic neuroimmune disorder affecting brain, spinal cord, and peripheral nerves.🧵
Warning Sign #1: The pandemic didn’t end - it just changed shape.
The virus keeps evolving. The acute symptoms may fade.
But for many, the infection never truly ends.
Even young, previously healthy people experience:
mental fog,
dizziness when standing,
sensory disturbances,
exhaustion after minimal effort,
racing heart.
That’s Long COVID.
Warning Sign #2: The virus leaves behind molecular debris - and the immune system won’t let it go.
Sometimes it’s spike protein fragments in the blood.
Sometimes viral RNA in the olfactory bulb or even the skull.
This triggers persistent immune alarms:
T cells get activated
Inflammation spreads to the brain
Neuronal connections start breaking down
The war continues - long after the virus is gone.
Warning Sign #3: The brain gets sick - even when standard scans look “normal.”
MRI often misses it. But PET imaging shows:
reduced glucose metabolism in the brainstem,
limbic inflammation,
microglia digesting synapses.
Patients say:
“I know what I want to say, but I can’t get it out.”
It’s inflammatory disruption of higher brain function.
Warning Sign #4: It’s not just the brain - the body’s autopilot system begins to fail.
The autonomic nervous system - which controls heart rate, blood pressure, digestion - goes haywire.
Blood pools in the legs; the brain is starved of oxygen.
POTS, dizziness, blackouts, heat intolerance
Even the vagus nerve - the main communication line between brain and body - shows structural damage in some studies.
Warning Sign #5: The immune system may start attacking the nervous system itself.
After infection, some people develop autoantibodies:
against adrenergic receptors,
against cholinergic synapses,
against neurons.
In experiments, these antibodies from Long COVID patients were transferred to mice - and caused neurological symptoms.
This isn’t just immune activation. It’s autoimmunity.
Warning Sign #6: Smell loss isn’t just a quirky symptom - it’s a red flag.
Olfactory tissue often shows:
inflammation,
neuronal destruction,
lingering T cells months after infection.
Even after viral clearance, the damage and local immune activity can persist - blocking recovery.
Smell loss may signal long-term damage to the central nervous system.
Warning Sign #7: Spike protein isn't just debris - it can fuel clotting and inflammation.
Persistent spike fragments have been found in blood and even skull tissue months post-infection.
They bind fibrin - form resistant microclots
These can obstruct capillaries, disrupt brain perfusion, and trigger microglial activation, cause ischemia-reperfusion injury
Even without active virus, brain tissue can be damaged by the aftermath of infection.
Warning Sign #8: SARS-CoV-2 may accelerate brain aging.
Evidence from autopsies, mice, and imaging shows:
damage to dopamine neurons,
loss of neurogenesis in the hippocampus,
inflammatory profiles resembling Parkinson’s and Alzheimer’s.
For some, COVID acts as an accelerant for neurodegenerative processes.
Warning Sign #9: No one is exempt. Not the young. Not the recovered.
Reinfections raise the risk.
Immunological imprinting may alter long-term responses.
Long COVID is not rare - it’s the aftermath of a system-wide disruption.
With no diagnostic test.
No cure.
And millions affected globally.
Bottom line: Long COVID isn’t “just fatigue.”
It’s:
chronic neuroinflammation,
immune dysregulation,
vascular dysfunction,
autonomic breakdown.
It’s a warning that infectious disease can leave lasting biological scars - not just in “high-risk” groups, but in anyone. @szupraha @ZdravkoOnline
Moen et al. (2025) - Neuroimmune Pathophysiology of Long COVID onlinelibrary.wiley.com/doi/10.1111/pc…

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More from @ZdenekVrozina

Dec 28
Your brain has a built-in cleanup system - the glymphatic system. Two recent papers point to the same theme. When this cleanup slows down, sleep and cognition often take the hit - and in Parkinson’s, impaired cleanup may also worsen toxic protein buildup🧵
Think of glymphatics as the brain’s plumbing. CSF (brain fluid) flows along blood vessels, mixes with fluid between cells, and helps wash out metabolic waste. It’s strongly tied to sleep, vessel pulsations, and astrocyte water channels (AQP4).
5-year post-COVID follow-up - 17 people who had COVID were followed at 1, 2, and 5 years after discharge. Researchers combined cognitive testing + sleep questionnaires with MRI glymphatic markers.
Read 18 tweets
Dec 27
Long COVID has been treated like a messy pile of symptoms.
This review proposes a cleaner frame - a self-sustaining immune loop - with monocytes/macrophages at the center🧵
That’s the paradigm shift.
Not post-viral damage + anxiety, and not one autoimmune disease for everyone,
but a chronic innate-immune state that can spill into many organs.
Why macrophages? Because they sit at the crossroads of
antigen handling, cytokines, endothelial activation, clotting signals, tissue repair, and neuro-immune crosstalk.
Read 24 tweets
Dec 27
COVID doesn’t have to kill neurons to change brain function. It can retune how neurons regulate their messages.🧵
A new PLOS ONE paper shows that SARS-CoV-2 leaves a measurable molecular footprint in the brain - specifically in how neurons process their mRNA
A lot of COVID brain talk is inflammation / clots / imaging. This paper zooms in on something quieter - but powerful. How brain cells finish their mRNAs!
Read 20 tweets
Dec 26
Could COVID affect fertility through immune cross-reactions? This isn’t just online speculation anymore. Researchers are testing it head-on - identifying specific antibodies and checking what they do in living organisms🧵
A new paper in Journal of Autoimmunity builds on a classic idea in immunology - molecular mimicry. Some short stretches of the SARS-CoV-2 spike protein may resemble parts of human proteins involved in reproduction.
The team previously mapped spike segments with notable similarity to spermatogenesis-associated proteins, then synthesized four short spike peptides (peptides 1-4). The first question was simple. After infection, do people develop antibodies that recognize any of these peptide segments?
Read 14 tweets
Dec 22
An interesting population-level signal is coming from Barcelona.
Antihistamines, Long COVID and thrombosis🧵
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.
Read 12 tweets
Dec 22
Immunity that once protected us from deadly infections
may now increase the risk of autoimmunity, Long COVID, and chronic inflammation.
A new review explains why🧵
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.
Read 17 tweets

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