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
This preprint shows how SARS-CoV-2 acts like a biological hacker - taking over our protein factories and silencing immune defenses.
It’s not just a respiratory infection. The virus reprograms the fundamental machinery of the cell - and that’s why its impact can linger.🧵
Remember when we learned Nsp1 alone could sabotage ribosomes? Yerlici et al., 2024.
The new preprint reveals SARS-CoV-2 goes even further - broadly reprograms translation to favor viral RNAs + silences immunity.
The main target: translation - the process where ribosomes build proteins from mRNA.
SARS-CoV-2 doesn’t just use it - it reprograms it, so instead of making protective proteins, the cell prioritizes viral ones.
New peer-reviewed study on the chronicity of COVID-19 in Viruses.
One of the authors? Former CDC director Robert Redfield.
The paper warns about persistence of SARS-CoV-2 in Long COVID - and doesn’t shy away from controversy.🧵
LC (PASC) = debilitating chronic disease.
10–20M in the US, >420M globally
200 symptoms, hitting 12 organ systems
No approved treatments
Affects kids, adolescents, healthy adults
Key message.
“Knowledge about chronic LC is still in its embryonic stage.”
Currently, there are more questions than answers.
A study just tested whether an old HIV drug - tenofovir (TDF/TAF) - could work against SARS-CoV-2 and even help with long COVID.
The lab results are striking: it strongly blocked the virus🧵
Tenofovir is a nucleotide analog - a fake building block for viral RNA.
Once inserted, it stops the virus from copying itself.
In experiments, this worked even at high viral loads.
The spotlight is on TAF.
More potent than TDF,
safer for long-term use,
and most importantly - it concentrates in lymphoid tissues (lymph nodes, spleen, immune cells).
A new 3-year follow-up study in Brain Communications tracked patients with post-COVID brain condition for 38 months.
What they found is a story of part compensation, part healing in the brain.🧵
At 6 months, people with post-COVID were still very tired.
Thinking was mostly fine, but attention and alertness were weaker.
Brain scans showed the frontal lobes working overtime - the brain was pushing harder to keep up. That’s early compensation.
At 23 months, there was progress, but not a cure.
Fatigue eased for some, others stayed stuck.
The brain started to spread the workload - brainstem, cerebellum, and temporal areas joined in. More networks pitched in to help - a reorganization phase.
One mystery of Long COVID - why immune cells get stuck in a harmful, inflammatory mode.
A new study shows the switch is metabolic - and a single checkpoint can decide whether Th17 cells protect or drive disease.🧵
In both children and adults with Long COVID, we see immune cells stuck in a harmful mode.
Among them - Th17 cells, which can either protect us or drive chronic inflammation.
A new study in Science Signaling, 2025 uncovers why these cells flip - and what keeps them locked in the pathogenic state.
Th17 cells have two faces -
non-pathogenic (protective, balanced),
pathogenic (autoimmune, chronic inflammation).
The critical switch? Cellular metabolism.
A massive new peer-reviewed review (161 studies, 2+ million patients) makes it clear.
COVID-19 isn’t just a respiratory infection.
It’s a multi-system disease leaving lasting scars on lungs, heart, brain, kidneys, and more.🧵
Among hospitalized patients the numbers are stark.
Lungs - 78% affected
Heart - 32%
Nervous system - 43%
Kidneys - 28%
Months later, 10-35% still live with organ dysfunction.
Why? The virus triggers:
a cytokine storm (immune system fire),
endothelial injury (blood vessels damaged),
micro-clots that choke tiny capillaries.