Zdenek Vrozina Profile picture
Nov 28 21 tweets 4 min read Read on X
SARS-CoV-2 causes long-lasting structural changes in the brain - even in people without symptoms.
Recovered ≠ normal. In this study, every single recovered participant still showed measurable abnormalities.
And this is 6-12 months after infection🧵
47 participants - Long COVID (19), recovered without symptoms (12), uninfected controls (16)
Multimodal 3T MRI - myelin (T1w/T2w), white matter microstructure (MD/AD/RD/FA), MR spectroscopy
Variant based on timing/location - Australia 2022–23, this was almost certainly Omicron
Headline?
Both post-COVID groups show clear structural brain differences.
Recovered often shows stronger myelin reorganization, while Long COVID shows more metabolic stress and some inflammation related diffusion patterns.
What does stronger myelin reorganization mean?
The T1w/T2w ratio reflects myelin content.
Long COVID - increased myelin signal in a few regions
Recovered - increased myelin signal across much broader areas
Controls - none of these patterns
This doesn’t look like demyelination.
It looks like repair/remyelination/glial activation.
Not necessarily functional
Key point.
Not necessarily functional means the brain may be producing new myelin or glial scaffolding,
but this does not guarantee a return to original signal quality or network efficiency.
Repair ≠ restoration.
Sometimes it’s compensatory wiring - keeps the system running, but less efficiently and at higher metabolic cost.
Long COVID = stronger metabolic and diffusion abnormalities.
Metabolism:
↓ Glutamine (immune and mitochondrial consumption).
↑ NAA (neurons trying to compensate for reduced efficiency).
Diffusion - patterns matching inflammation or tissue densification (MD↓) and rigidity/reorganization (FA↑), especially in SLF - a key pathway for attention and cognition.
LC brains show higher ongoing metabolic strain, slowing or distorting repair.
Recovered = faster, but not guaranteed better repair.
Recovered participants show
less metabolic strain
more extensive myelin remodeling
evidence of large scale reorganization of white matter pathways
This might reflect a faster compensatory repair response, but not necessarily a return to the original architecture.
Two different ways the brain adapts to the same viral insult.
Imaging aligns with symptoms.
More myelin in temporal regions = better physical function
Less myelin in midbrain = worse cognitive performance
Cognitive symptoms are not psychological - they map onto structural and metabolic changes.
Sum:
SARS-CoV-2 disrupts myelin regulation (similar to known neurotropic viruses)
Leaves a measurable footprint months after recovery
Long COVID and recovered follow different repair trajectories
Brain repair can be partial, maladaptive, energetically expensive
These changes persist (for now months after infection)
What this shows.
SARS-CoV-2 has long-term neurobiological effects
Recovered ≠ normal - all recovered showed measurable abnormalities
LC ≠ recovered - different stress patterns, different compensations
Affects networks for attention, cognition, motor control, alertness
Long COVID is a measurable neurological condition, not a functional or psychological syndrome
Thapaliya et al., Altered Brain Tissue Microstructure and Neurochemical Profiles in Long COVID and Recovered COVID-19 Individuals (2025, pre-proof). sciencedirect.com/science/articl…
We’re not saying SARS-CoV-2 is the new HIV etc
But we are saying this -
The mechanisms SARS-CoV-2 uses in the brain overlap with viruses that do produce long-lasting neural changes.
Spike - activates microglia, alters astrocyte metabolism
N protein - drives inflammatory cascades
ORF proteins - disrupt mitochondrial function
Nsp1 - blocks ribosomes, limiting the cell’s ability to produce proteins needed for neuronal repair and myelin maintenance
These mechanisms naturally produce the kinds of MRI patterns we see
glial activation
myelin remodeling
rigid or reorganized white matter pathways
metabolic stress in neurons
These are not random MRI quirks.
These are exactly the changes you’d expect from a virus whose proteins block ribosomes, overload glia, and destabilize neuronal metabolism.
Time is passing - and we still refuse to learn from the biology of viruses (proteins) like HIV.
And one last question we should dare to ask.
What will the brains of children look like if we deliberately leave them without any protection against repeated SARS-CoV-2 infections?
From everything we already know - MRI, EEG, immune markers, neuroinflammation, metabolic profiles, developmental studies - several biologically plausible trajectories are already visible.
Every single one of them points to the same thing - a failure of public health. @szupraha @ZdravkoOnline @adamvojtech86
To be precise - the MRI abnormalities in the recovered group were group-level effects.
With only 12 participants, a result this strong almost certainly reflects a broad signal across the group - even though the design can’t determine each individual.
So instead of “all 12,” the correct interpretation is -
“almost everyone in the recovered group showed measurable differences compared to controls.”

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More from @ZdenekVrozina

Nov 29
Cognitive PASC (COVID brain fog with measurable cognitive decline) isn’t just another flavor of long COVID.
This new important study shows its a biologically distinct condition that carries features resembling early neurodegenerative processes - even after mild COVID🧵
Evidence of brain injury in cognitive PASC -
The cognitive PASC group shows clear signs of astroglial injury
elevated GFAP (astrocyte damage marker)
NfL not elevated, meaning no widespread axonal destruction
This suggests a chronic, low-grade neuroinflammatory–degenerative stress.
Structural changes in the cerebral cortex -
MRI reveals cortical thinning in regions essential for attention, memory and integrative processing
the cingulate cortex
the insula
the parahippocampal region
These are the same regions commonly affected in early neurodegenerative conditions.
Read 16 tweets
Nov 29
COVID can cause a long-lasting breakdown of immune homeostasis, where elevated IL-7 and IL-15 keep T cells activated for months after the acute infection.
In some people this dysregulated state becomes persistent - and may directly contribute to long COVID🧵
This is an important shift in understanding. It’s not just that T cells stay activated - the key question is why.
The new study shows that the drivers are homeostatic cytokines that normally help rebuild the T-cell pool after infection.
The problem is that COVID causes a major loss of T cells (lymphopenia).
The body responds by ramping up IL-7 and IL-15 to help replenish them.
But these cytokines become so abundant that T cells remain on standby for months - even long after the virus has cleared from the airways.
Read 18 tweets
Nov 27
SARS-CoV-2 spike can trigger Sjögren-like damage in salivary glands - and the parallels with HIV are striking.
Salivary glands are not passive tissue. They’re immune active organs with TLR2/4, resident lymphocytes, and epithelial cells that behave like mini immune sensors🧵
A new study shows something interesting. The SARS-CoV-2 spike protein alone - without virus, without ACE2 entry - can cause significant damage to submandibular glands, closely resembling early Sjögren’s disease.
Mice injected with spike showed a sharp drop in saliva production. Histology revealed lymphocytic infiltrates around ducts and vessels - the same architecture seen in autoimmune sialadenitis.
Read 15 tweets
Nov 26
A new 3-year scRNA-seq study shows something striking. Some people after COVID still carry an immune profile that looks like accelerated aging - low naive T cells and persistent activation of pathogenic Th17. Not a long-COVID cohort, but biologically very close🧵
The study didn’t select people with long COVID.
It followed 47 individuals after COVID-19 for 3 years - and some symptoms were reported within the cohort, allowing the authors to examine symptom-associated immune signals without defining a long-COVID subgroup.
The first major finding.
Even after 3 years, three key protective cell types remain significantly reduced
naive CD4 T cells
naive CD8 T cells
SLC4A10+ MAIT cells
This pattern is normally associated with immunosenescence.
Read 20 tweets
Nov 24
When we look at the brain after COVID, we need to accept something that still hasn’t fully landed in public understanding - changes in cerebral perfusion aren’t limited to people with Long COVID. They show up in almost everyone.
And this new study makes that point clear🧵
What the authors demonstrate is simple but essential - the perfusion changes they found aren’t exclusive to PCC patients - they also appear in the controls, who had COVID but don’t report chronic symptoms.
So when we compare PCC patients with post-COVID controls, we’re not comparing a sick brain to a healthy one.
We’re comparing a COVID-affected brain to another COVID-affected brain.
And that fundamentally changes how we have to read the results.
Read 19 tweets
Nov 22
This study shows something striking.
The spike protein by itself can trigger ACE2-targeted autoimmunity - causing lung and kidney injury without any viral infection.
This may help explain why COVID-19 can damage organs even when no virus is detectable in the tissue🧵
Researchers immunized Wistar rats with recombinant SARS-CoV-2 spike protein.
Control animals received the same adjuvant (IFA).
The only difference was the spike antigen itself.
70% of the animals developed anti-ACE2 antibodies, and - interestingly - these appeared earlier than anti-spike antibodies.
That’s classic idiotype–anti-idiotype immunology.
Read 21 tweets

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