A new preprint study shatters the idea that pediatric long COVID is just a mild or different version of the adult form.
It shows that children share the same core immune patterns - and, strikingly, some resemble those seen in chronic infections like HIV.🧵
The paper message is clear - pediatric LC is biologically defined immune dysfunction.
Children display
shifts in monocytes (↑ non-classical, ↓ CCR6),
T cell changes (↑ Tregs, ↓ central memory CD4, exhausted CD8),
exhausted B cells.
At the root lies a failure of antigen-presenting cells (monocytes & dendritic cells).
Normally, they carry viral information to T and B cells. But in LC, they express less CCR6/CCR7 - they can’t migrate properly to lymph nodes or activate adaptive immunity.
“Suppressed expression of CCR6 and CCR7… could impair antigen presentation and adaptive immunity.”
The consequence?
B cells don’t mount a strong antibody response.
Children with LC had significantly lower anti-RBD IgG and IgA titers, and their antibodies neutralized the virus less effectively.
The virus can persist in tissues, like the gut.
Meanwhile, T and NK cells become hyperactivated.
On the surface this looks like a strong immune defense. But in reality, it’s a dead end.
These cells show exhaustion markers (PD1, CD57, CD38, HLA-DR↑).
“Elevated expression of activation and exhaustion markers…”
A vicious cycle?
Persistence - activation - exhaustion - persistence again.
And here’s the striking part - the authors explicitly point to parallels with HIV.
“Elevated CXCR3 expression on CD8 TCM has also been reported in people living with HIV-1, suggesting a shared trait of chronic viral infections.”
The same is true for B cells.
Cluster 15 B cells show an exhausted-like phenotype -
“…commonly observed in chronic viral infections such as HIV-1.”
SARS-CoV-2 can imprint the immune system in children in ways that mimic chronic viral disease.
In pediatric LC, CD8 stem-cell like memory T cells (TSCM) decreased, while central memory T cells (TCM) increased.
And within TCM, there was a shift toward CXCR3+/CCR6+ cells - a phenotype of chronic stimulation.
The clinical point is sobering.
Weak antibodies + exhausted T/NK cells = a recipe for viral persistence.
When APCs don’t work (CCR6/CCR7↓), B cells never make high-quality antibodies.
The virus hides, the immune system pushes harder, and burns itself out.
The result?
A state of chronic immune imbalance.
Maybe less dramatic than HIV, but uncannily similar.
Pediatric LC emerges as a model of chronic viral immunopathology - not a psychological aftermath, but a biological condition with measurable immune signatures.
And perhaps we won’t need to argue about these parallels for long.
The authors themselves are already drawing them - between pediatric LC, adults with LC, and chronic infections like HIV.
Pujol et al., 2025. Pediatric Long COVID Is Characterized by Myeloid CCR6 Suppression and Immune Dysregulation. biorxiv.org/content/10.110…
Dobře si to přečtěte @szupraha @ZdravkoOnline @msmtcr @Hygiena_cz. LC je dnes nejčastější chronické onemocnění u dětí - překonává astma.
Tohle jsou následky vaší nečinnosti.
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