A study comparing the immune system 3 months after COVID-19 and after influenza shows something clear.
SARS-CoV-2 leaves behind a far deeper and longer-lasting immune imprint than seasonal flu.
And the difference isn’t subtle🧵
Researchers used high-dimensional 40-marker CyTOF to map dozens of immune cell types in detail.
The result was so distinct that machine-learning models could accurately classify post-COVID vs post-flu individuals (AUC > 0.95).
The biggest differences appeared in chemokine receptors - the navigation system that tells immune cells where to go.
Post-COVID patients showed markedly increased CXCR3 and CCR6 across multiple lymphocyte populations (T, NK, pDC, monocytes).
This is a unusual and consistent signature.
CXCR3 and CCR6 are not minor markers.
They are the GPS of the immune system.
In post-COVID patients, it is still dialed toward inflamed tissues, especially the lungs.
The body is behaving as if the threat hasn’t fully passed.
This means -
persistent tissue-homing = prolonged low-grade inflammation.
Months after infection, the immune system remains mobilized instead of returning to baseline.
Now the contrast with influenza.
Post-flu patients mainly showed a decrease in CCR4 - a mild, transient pattern consistent with normal recovery.
Influenza does not produce long-lasting chemokine activation.
It does not keep immune cells in a go to tissues mode.
It does not mirror the post-COVID immune state.
Simply -
Influenza leaves behind small footprints.
COVID-19 rewires immune cell trafficking.
The two infections leave completely different immune landscapes.
Most interestingly, the study identified two distinct immunological subgroups within the post-COVID cohort.
The strongest chemokine abnormalities - highest CXCR3/CCR6 levels, most intense tissue-homing - were found in younger individuals.
And this happened even in people with no long COVID symptoms.
That’s a important message.
Feeling recovered ≠ immune system actually returning to normal.
Young immune systems react strongly to SARS-CoV-2, and their hyper-migratory profile persists long after symptoms resolve.
Hidden immunological dysregulation in people who feel perfectly fine.
These differences were not explained by severity of the original infection, hospitalization duration, treatments received (steroids, antivirals, immunomodulators), presence or absence of long COVID
The only factor that distinguished the post-COVID subgroups was age.
This supports the idea that SARS-CoV-2 creates a multisystem, long-lasting immune imprint, particularly visible in chemokine signaling and cell trafficking.
Migration - persistent influx of immune cells into tissues - potential ongoing dysfunction.
Why is COVID-19 so different from flu?
Because SARS-CoV-2 has a much broader tropism. Brain, lungs, heart, vessels, immune cells, kidneys, gut..
This creates a multi-organ immune signature that influenza simply doesn’t generate.
Sum:
COVID-19 leaves the immune system in a state of extended activation and redirected trafficking, still behaving as if it’s hunting the virus.
Influenza does not.
The strongest abnormalities appear in younger individuals - even those who believe they have fully recovered.
This study adds to growing evidence that COVID-19 is not immunologically equivalent to influenza.
The post-infection immune system behaves like it experienced a multisystem viral event, not a simple respiratory illness.
Pérez-Cózar et al., High-Dimensional Immunophenotyping of Post-COVID-19 and Post-Influenza Patients Reveals Persistent and Specific Immune Signatures After Acute Respiratory Infection. Journal of Medical Virology 2025. onlinelibrary.wiley.com/doi/10.1002/jm…
@szupraha (esp Kynčl)
Další důkaz, že tvrzení covid je jako chřipka bylo od začátku nepravdivé.
Rizika jste nepopsali poctivě.
Dlouhodobě vytvářeli dojem, že covid je běžná respirační infekce, což zjevně není.
Výsledkem byla zavádějící komunikace, která poškodila veřejné zdraví.
@ZdravkoOnline @adamvojtech86
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A new observational study examined whether metformin prescribed within the first week of SARS-CoV-2 infection reduces the risk of Long COVID - what it actually shows🧵
The authors used N3C electronic health records and a target trial emulation design to compare metformin vs several other COVID-related prescriptions.
After weighting, both groups had ~248 people.
The outcome was Long COVID (ICD-10 U09.9 or a computable phenotype) or death within 180 days.
A new review breaks down what SARS-CoV-2 ORF/accessory proteins actually do - from interferon suppression to mitochondrial disruption. Here are the key points, followed by how some of these mechanisms compare to those used by HIV🧵
A new review makes something very clear.
SARS-CoV-2 doesn’t rely only on spike. It uses a broad arsenal of accessory proteins (APs) that shape
how severe the acute phase becomes,
which organs are affected,
and the biological conditions that make long-term sequelae more likely.
These proteins aren’t side notes - they’re central modules of pathogenesis.
The review goes protein by protein and shows a pattern we haven’t had clearly assembled before.
SARS-CoV-2 runs a multi-layer immune-evasion network.
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.
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.
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.
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.