When we talk about COVID in children, we often hear - mild disease.
The real question we rarely ask is this - what if some children leave the infection with a silent, measurable cardiovascular footprint - and we simply don’t have long enough follow-up yet to see what it leads to?🧵
About a quarter of children.
In a new study, 16 out of 67 kids (24%) had subclinical cardiac contractility changes three months after mild or asymptomatic COVID - despite having no persistent symptoms.
The abnormalities were detected only with speckle-tracking strain imaging, a sensitive method that can reveal very subtle myocardial dysfunction.
But the most important finding was not the heart itself.
It was the immune signature that distinguished the affected children.
The key signal?
Children with subclinical dysfunction had significantly fewer regulatory T cells (Tregs) - the immune system’s main braking mechanism
What do Tregs do?
They help limit excessive inflammation, maintain balance between immune defense and tissue damage, coordinate cellular and antibody responses.
When Tregs are reduced, immune activation can persist longer and become less controlled.
In this study, lower Tregs were linked to
ongoing CD8 T-cell activation
weaker coordination with neutralizing antibodies
higher inflammatory signals
Together, this suggests a pattern of impaired immune regulation.
So a dysregulated immune response that may leave a subtle functional imprint on the myocardium even after mild infection.
There were also hints that affected children had higher initial viral loads and a trend toward shorter immune cell telomeres - both consistent with more intense or prolonged immune activation.
Importantly, none of the children had long-COVID symptoms!
This is a subclinical signal - detectable only with sensitive testing.
The key question is not whether they are ill now, but what this means over time.
Although published in 2026, the cohort reflects early-pandemic infections.
When we place this study alongside others, a broader picture emerges.
Different teams are looking at different layers of the same phenomenon.
Di Chiara examined children ~3 months after infection using strain imaging and deep immune profiling.
A subset has subtle myocardial dysfunction and these children share a distinct immune pattern - especially low Tregs.
Karaviti 2026 looked at children up to one year after infection using GLS strain.
It found persistent strain reduction, particularly after more severe illness, and evidence of endothelial activation.
This adds a vascular dimension to the story. sciencedirect.com/science/articl…
Children after COVID-19 had persistently reduced GLS
= a sign of subclinical myocardial dysfunction
Even though they were otherwise healthy.
Kim 2025 took a different approach.
It focused on ECG findings, blood pressure regulation, and arrhythmias over a longer time frame (2–3 years).
It showed that some children develop electrical and autonomic abnormalities. researchgate.net/publication/39…
Taken together, these studies suggest multiple possible layers
myocardial mechanics (strain)
vascular/endothelial activation
autonomic and electrical regulation
These are not contradictions - they may be different expressions of the same underlying process.
What Di Chiara adds is a plausible biological link -
when immune braking is reduced (Tregs ↓), persistent activation and inflammation may continue - potentially affecting cardiovascular function even after mild infection.
And this is the real public-health question.
We do not know whether these findings resolve, remain stable, or progress.
But they show that a measurable signal can persist months - and sometimes years - after infection.
Why does this matter?
Because in adults, even small changes in strain can precede overt cardiovascular disease by many years.
If similar patterns exist in children, we may be seeing the very early stage of a long trajectory that we are not yet tracking systematically.
It does mean something important.
Some children may carry a subtle cardiovascular imprint of infection into adolescence and adulthood - and we currently lack long-term surveillance data.
Different countries, different cohorts, different methods - yet a consistent theme emerges - measurable, silent cardiovascular changes after COVID-19.
@szupraha @ZdravkoOnline @adamvojtech86 @adamkova_vera
Costanza Di Chiara at al., Impaired Treg Response and Subclinical Cardiac Dysfunction in Children Following SARS-CoV-2 Infection. journals.lww.com/pidj/fulltext/…
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The interesting proof-of-concept study shows that in some severely immunocompromised people with long-lasting COVID-19, it is possible to use autologous VSTs🧵
It is possible to -
Produce SARS-CoV-2–specific T cells from their own blood (autologous VSTs),
Infuse them back into the patient,
In the 3 treated patients this was temporally associated with clinical improvement, PCR turning negative, and better CT findings - without serious side effects.
How strong is the evidence of effectiveness?
Rather weak to moderate for efficacy, but fairly solid for feasibility and short-term safety. This is an early signal, no control group.
One overlooked signal of the pandemic. IL-32 - a cytokine known from HIV research as a marker of chronic immune activation - is now elevated not only in COVID patients, but across large parts of the general population🧵
Here’s an underappreciated detail. IL-32 isn’t just another inflammatory cytokine. In HIV research, it’s a well-known marker of chronic immune activation - linked to persistent low-grade inflammation and long-term viral persistence
In people with HIV, IL-32 doesn’t simply fight infection. It can also upregulate immunosuppressive pathways (PD-L1 and IDO1), creating an environment where inflammation persists - but effective viral clearance does not.
When the precautionary principle is not applied to pregnancy and brain development, it fails its purpose.
An informed framework and systematic follow-up should have come earlier - and are still needed🧵
One more study in a long line of findings adds hard endpoints
neonatal brain MRI
standardized developmental testing at age 2.
The finding is fundamental.
Prenatal exposure to SARS-CoV-2 was associated with measurable differences in brain structure shortly after birth.
SARS-CoV-2 may leave a long-lasting population imprint - not a dramatic cytokine storm, but a quiet, low-grade, atypically regulated inflammatory background. One measurable signal of this may be the cytokine IL-32🧵
In a new study of 1,000 healthy blood donors and 212 hospitalized COVID-19 patients, researchers found IL-32 levels were significantly higher not only in severe cases, but across the general population during the pandemic.
This suggests something important. Even outside diagnosed illness, widespread viral exposure left measurable biological traces - a sign of subclinical, population-level immune activation.
New study in Nature Aging.
Metformin slows inflammatory aging through a completely unexpected mechanism.
This isn’t just about metabolism.
It’s about misplaced DNA.🧵
In aging and senescent cells, fragments of chromatin can break off and leak into the cytoplasm.
These are called cytoplasmic chromatin fragments (CCFs) - essentially pieces of our own DNA in the wrong place.
The immune system treats this misplaced DNA as a danger signal.
CCFs activate the cGAS-STING pathway, a core innate immune sensor, triggering chronic sterile inflammation - one of the key drivers of inflammaging.
COVID as a neurovascular brain problem. A new study shows impaired regulation of cerebral blood flow during mental exertion.
In patients with long COVID, this finding was associated with worse cognitive performance🧵
Important context - long COVID patients were assessed at an average of ~314 days after infection (10 months).
The study did not specify the viral variant, but based on timing, some infections may have occurred during the Omicron era.
The authors examined activity in the prefrontal cortex (region crucial for attention, working memory, and executive function) using fNIRS, a method that indirectly tracks changes in cortical blood oxygenation during tasks.