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

Jun 16
What connects HIV and SARS-CoV-2 in the brain?
Not structural homology - but functional parallels between viral proteins that can drive chronic neuroinflammation and immune evasion.
A short thread on Tat, viroporins, ORF8, and viral neuropathogenesis. @dbdugger 🧵
COVID-19 (Long COVID) is associated with:
microglial activation
blood-brain barrier (BBB) disruption
persistent viral antigens
memory and attention deficits
These are also key features of HIV-associated neurocognitive disorder (HAND). What’s the link?
In HIV, the Tat protein is central to neuropathology:
secreted from infected cells
crosses the BBB
activates microglia via TLR4
triggers IL-6, TNFa, ROS
promotes excitotoxicity in neurons
Tat = neurotoxic transcriptional regulator.
Read 14 tweets
Jun 12
In recent months, a growing number of robust scientific studies have confirmed that even mild SARS-CoV-2 infection is not biologically neutral in children. Two new studies reveal surprising depth of impact - metabolically and immunologically.🧵
For years, pediatric COVID-19 was framed as "mild."
But a large metabolomic study (Lawler et al., 2025) shows that even children with mild symptoms show significant systemic changes in their blood - and a newer study (Gaebler et al., 2025) suggests some of these changes persist.
Lawler et al. analyzed 147 children
55 had acute COVID-19 (most were not severely ill)

Findings revealed marked alterations in:
lipid metabolism (↓HDL, ↓ApoA1, ↑triglycerides)
inflammatory proteins (↑GlycA)
amino acid-related metabolites
Read 12 tweets
Jun 10
What if time really started ticking faster after COVID?
Renner et al. (2025) and a new @PolyBioResearch - supported study both show:
Post-COVID immune activation may silently age the body, damage organs, and reduce resilience.
Let’s connect the dots.
@dbdugger @RealCheckMarker @1goodtern
Renner et al. (2025) studied 68 patients with Long COVID.
Most of those with moderate/severe symptoms showed:
Persistent CD8+ T cell activation
Loss of naive T cells
High IL-3 (a hematopoietic inflammatory signal)
It’s immune rewiring. sciencedirect.com/science/articl…
These immune changes correlate with gradual damage to ACE2-rich organs (drug-metabolizing):
Kidneys
Liver

That means potential trouble for:
Blood pressure meds (ACEi/ARBs)
Antidepressants, hormones, NSAIDs
Vaccines
Metformin
Even paracetamol...
Read 14 tweets
Jun 9
What do HIV and COVID have in common?
A lot more than you'd expect. Both viruses target the same key neuronal protein - TDP-43 - involved in ALS and other neurodegenerative diseases.
And both viruses have evolved to silence a major immune alarm system. @dbdugger @RealCheckMarker
TDP-43 is a protein that helps regulate RNA in cells.
When it's damaged or cleaved, it tends to accumulate and form sticky clumps, which in turn damage neurons.
It’s a known hallmark in ALS, frontotemporal dementia (FTLD), and sometimes Alzheimer’s.
SARS-CoV-2 cleaves TDP-43. In 2023, researchers showed that SARS-CoV-2’s main protease (Nsp5) cuts TDP-43 into fragments.
These fragments are poorly soluble and form toxic aggregates - a first step toward neurodegeneration. nature.com/articles/s4139…
Read 10 tweets
Apr 30
Polybio: Nová studie o Long Covidu (Nature Immunology, 2025) přichází s biologickými podpisy Long Covidu spojeného s dušností. Výsledky ukazují poškození plic, zánět, známky srdečního stresu a nepřímý silný důkaz perzistence 👇
Studie analyzovala krevní plazmu lidí s Long Covidem z 🇬🇧 a 🇸🇪. Porovnali je se zdravými po covidu a zaměřili se na lidi s výraznou dušností - proč mají potíže s dechem i když mají „normální nálezy“.
Našla specifickou signaturu proteinů, která souvisí se zánětem, apoptózou a poškozením plic
CD40
IL-18
IKBKG (NEMO)
IRAK1
CCL3
Tyto proteiny aktivují signální dráhy jako NF-κB a TNF.
Read 19 tweets
Apr 29
Studie (Kratzer et al., Allergy 2024) ukazuje, jaké
COVID-19 zanechává dlouhodobé jizvy na imunitním systému - i po mírné infekci. ⚠️👇
10 měsíců po první nákaze

Pokles T, B, NK buněk.
Výrazná ztráta 50-60% nových T buněk z thymu (RTE).
Přepnutí imunity z Th1 (antivirová) na Th2 (alergická).
Ztráta neutralizačních protilátek.
Thymus normálně obnovuje náš imunitní repertoár.
Po COVID-19 ale výrazný pokles recent thymic emigrants (RTE) znamená, že tělo produkuje méně "čerstvých" T-buněk.
Zvláště rizikové pro děti a mladé lidi.
(Čína plošně nabídla Azvudine - lék podporující thymus.)
Read 13 tweets

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