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
A heart attack after COVID may not look like the classic heart attack we usually imagine.
A new core-lab study of patients with NSTEMI + COVID-19 suggests something more diffuse. Not just one blocked artery, but a blood-clotting and vessel inflammation problem🧵
First, two key terms.
STEMI is the type of heart attack where the ECG shows ST-segment elevation. It often means a major coronary artery is suddenly blocked.
NSTEMI is a heart attack without that classic ST elevation. It can be less obvious on ECG, but it is not minor.
So STEMI is often like a main pipe suddenly being blocked.
NSTEMI can be more complex. Partial blockage, smaller clots, multiple narrowed vessels, poor microvascular flow, or the heart being stressed by illness.
But COVID can add another layer.
For 2025, the societal cost of Long COVID and ME/CFS in Germany is estimated at €64.4 billion - about 1.44% of GDP.
For Czechia, this would roughly translate to around CZK 120 billion per year if we apply the same share of GDP - 1.44% of the Czech economy.
A simple population-based conversion would produce a higher number (200 billion), but that is an overestimate.
This should matter to you, @strakovka.
Because this is what poor public health policy costs. Ignoring prevention, ventilation, surveillance, post-COVID care, and the long-term damage caused by repeated infections.
A new systematic review looked at what happens to the heart after COVID - not during the acute infection, but months later.
The key point:
A normal ejection fraction does not always mean the heart is completely unaffected.🧵
In people assessed more than 12 weeks after PCR confirmed COVID - especially those with persistent cardiopulmonary symptoms - there is evidence of subtle, and sometimes persistent, cardiac involvement.
This may show up as
higher BNP/NT-proBNP
reduced LV-GLS
abnormalities on cardiac MRI
while LVEF often remains normal
Exertion and PEM.
A new paper studied people with long COVID using a 2-day (!) submaximal CPET protocol, combined with NIRS measurement on the calf muscle.
The authors looked at what happens to breathing, performance, and muscle oxygenation during repeated exertion🧵
The key finding.
In the long COVID group, muscle tissue oxygen saturation (TSI%) initially increased during exercise, but it did not stay elevated for as long as it did in controls. (Thomas 2026)
On day 2, this pattern was even worse. In long COVID, TSI% stayed above resting levels for a shorter period, while controls maintained elevated muscle oxygenation more effectively during exercise.
COVID-19 creates a state of immune dysregulation where the body may lose control over things it normally keeps suppressed - latent viruses, especially herpesviruses, and possibly even dormant cancer cells.
A new study on EBV and CD8 T cells fits into this bigger picture.🧵
The point is not simply that EBV can reactivate during COVID. We already have quite a lot of evidence for that.
In hospitalized patients with acute COVID, EBV reactivation was very common - around 68-73% - and it was seen not only in critical cases, but also in moderate disease.
The authors looked at EBV, CMV, HHV-6A and HHV-6B.
EBV dominated.
CMV and HHV-6B were detected only at low frequencies.
HHV-6A was not detected at all.
So this does not look like just random viral noise. EBV stands out.
In this cohort, children exposed to SARS-CoV-2 in utero showed higher rates of developmental delay and were also more likely to screen positive on an autism screening tool than pre pandemic controls🧵
The developmental delay signal comes from the group’s earlier work in the same cohort. In the abstract, the authors cite a rate of 11.6% in 172 exposed children versus 1.6% in 128 pre pandemic controls.
The newer clinical piece in this paper is the autism screening result. Among 218 SARS2 exposed children, 22 screened positive on M-CHAT-R/F (10.1%). In the control group, 30 of 527 screened positive (5.7%).