New preprint from Harvard & Massachusetts General Hospital -children with Long COVID show markedly increased levels of fibrinaloid microclots in their blood!
The highest levels appear in those with persistent SARS-CoV-2 spike protein in circulation🧵
Long COVID affects roughly 1 in 5 children after SARS-CoV-2 infection.
Common symptoms include fatigue, brain fog, pain, and shortness of breath.
Diagnosis remains largely clinical - we still lack objective lab biomarkers for pediatric LC.
To address this, the team led by Daniel Irimia and David Walt developed a microfluidic device that can quantifyfibrinaloid microclots - tiny, fibrin-like clots resistant to normal breakdown (fibrinolysis).
These structures can obstruct microcirculation and reduce tissue oxygen delivery.
Participants.
45 children and young adults with Long COVID (mean 17)
14 healthy pediatric controls
Samples collected March 2023 - November 2024
= most infections occurred during the Omicron era (BA.5 - JN.1).
All LC participants met CDC’s Long COVID criteria - symptoms persisting ≥3 months post infection, often lasting 6–12 months.
So - these were post-acute, not acute cases.
Results.
Long COVID 166 ± 107 microclots/sample
Healthy controls 61 ± 48
LC with detectable spike protein 229 ± 111
That’s more than a 3x increase in microclot burden in LC vs controls.
The new device performed remarkably well.
AUC = 0.94 (94% accuracy) at a threshold of 75 microclots/sample
Traditional manual counting under a microscope - only 66% accuracy (AUC = 0.66)
This microfluidic assay could become a screening tool for Long COVID.
The most intriguing finding.
Children with detectable SARS-CoV-2 spike protein in plasma had the highest microclot counts.
Spike antigenemia was measured using ultrasensitive Simoa assays.
This test - developed by David Walt’s lab (Harvard, Wyss Institute) - can detect full-length spike protein at picogramlevels, months after infection.
It has been validated in prior studies.
Detection of spike protein months later suggests persistent viral antigen release - likely from tissue reservoirs (gut, endothelium, immune cells).
Microclot formation appears linked to this ongoing antigenemia and chronic microvascular inflammation.
Importantly, the authors caution that these fibrinaloid microclots do not respond to standard anticoagulant therapy.
So their presence should not be treated as a typical clotting disorder - it reflects a distinct, pathological process of fibrin misfolding and immune activation.
Interestingly, even LC children without detectable spike protein showed elevated microclot counts -
suggesting either intermittent antigen release below detection limits,
or that microclots can persist longer than spike itself.
Authors conclude:
“The increased microclot burden in pediatric LC supports the role of microvascular dysfunction and persistent viral antigens in pathogenesis.”
In plain terms - pediatric Long COVID has measurable, biological signatures.
While still a preprint (not peer-reviewed), this study is important because it:
Provides a quantitative biomarker for pediatric LC,
Links microclots to persistent spike antigenemia,
Warns that these clots are anticoagulant-resistant.
Pediatric Long COVID shows measurable microvascular pathology tied to persistent viral antigens -
and quantifying microclots may finally offer an objective diagnostic tool. @szupraha @ZdravkoOnline
Irimia at al., Quantification of fibrinaloid clots in plasma from pediatric Long COVID patients using a microfluidic assay. researchsquare.com/article/rs-748…
Why it matters.
Microclots are not detectable by standard lab tests (like D-dimer).
And because they don’t respond to common anticoagulants, they can easily escape clinical attention.
Without recognition, fatigue and cognitive dysfunction may persist without an obvious cause.
These fibrinaloid microclots form an abnormal, amyloid-like version of fibrin.
They trap inflammatory proteins, cytokines, and complement factors -
creating a self-sustaining cycle of inflammation, microvascular obstruction, and oxidative stress.
Over time, this can impair oxygen delivery to tissues - especially the brain, heart, and muscles, where energy demand is high.
Persistent spike may maintain this process by chronically activating endothelial and immune cells = microvascular inflammation without large-vessel clots.
A silent, systemic pathology that standard medicine isn’t built to detect yet.
In children, prolonged microvascular dysfunction may carry long-term risks.
Impaired cognitive development, reduced exercise tolerance, and accelerated vascular aging.
That’s why studies like this one mark a turning point - translate invisible biology into measurable evidence.
Public health should have an answer to this.
Children showing measurable microvascular injury and persistent viral antigens need monitoring, not dismissal.
No screening protocols, no follow-up clinics, no guidance.
Families are left to navigate a biological condition that health systems barely acknowledge. @szupraha @ZdravkoOnline @adamvojtech86
Yes it’s a new method, and it still needs validation.
But the biology it reveals isn’t new anymore.
Persistent spike and microvascular injury have now been shown by multiple independent teams.
What’s missing isn’t evidence - it’s acknowledgment.
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COVID-19 doesn’t just cause inflammation.
It switches off the genes that repair blood vessels - and switches on those that drive inflammation and destruction.
And what’s worse - this state lasts for at least six months, long after the infection is gone🧵
Researchers studied endothelial progenitor cells - the special cells that normally repair blood vessels after injury.
In people recovering from severe COVID (before vaccines even existed), they found these repair cells were genetically reprogrammed.
The healing genes were switched off.
NOS3 - produces nitric oxide to relax vessels
KLF2 - master regulator of endothelial health
ANGPT1, TGFB1, SMAD6 - maintain vessel stability and repair
The body’s vascular repair system went silent.
The study, conducted in a mouse model, shows that SARS-CoV-2 infection can alter epigenetic information in sperm - specifically the profile of small noncoding RNAs passed on at fertilization - and that these changes can be transmitted to the offspring🧵
These changes may influence the development of the nervous system and the stress response of the offspring, independently of the DNA sequence itself.
Male mice infected with SARS-CoV-2 were mated with uninfected females four weeks after recovery.
Their offspring showed no signs of infection, but exhibited changes in behavior and gene expression.
COVID didn’t end - it changed the baseline of how often people fall ill, miss work, and drop out of the labor force. A new JAMA study shows the US now lives in a permanent flu-season mode, all year round🧵
COVID-19 has created a new year-round baseline of illness - its effects persist even without major waves or restrictions, pointing to chronic impacts from ongoing infection or post-infectious conditions, including long COVID.
This new health environment means lower productivity and a greater need for worker protections such as paid sick leave, improved ventilation, and infection prevention at workplaces.
Post-COVID depression isn’t weakness.
It’s biology.
A landmark, important study shows how the virus leaves a measurable molecular trace - in the very proteins that protect your brain from degeneration🧵
A new study in Translational Psychiatry shows that psychiatric symptoms after COVID-19 aren’t just psychological.
They have a biological signature - measurable changes in blood proteins linked to the brain, metabolism, and immunity.
People who developed new depression, anxiety, PTSD, or insomnia after COVID showed distinct biochemical profiles compared to those who recovered fully or had other long COVID symptoms.
It’s not psychology.
It’s neurobiology.
7-12% of patients recovering from moderate to severe COVID-19 show persistently low counts of B cells, CD4 T cells, and Tregs, even after clinical recovery.🧵
This sustained adaptive immune deficit may represent a important mechanism underlying Long COVID, resembling immunological patterns seen in chronic infections such as HIV and EBV.
The authors highlight a possible link with low serotonin levels, which support B and T cell proliferation - a hypothesis drawn from the work of Wong et al., 2023.
Yes, we wrote about this study. It is important.
A study from Cambridge in Brain shows that even months after COVID-19, survivors still carry measurable inflammation-related changes in the brainstem - the part of the brain that keeps you breathing, awake, and alive🧵
Using ultra–high-field 7 Tesla MRI, researchers found abnormal magnetic signals (quantitative susceptibility mapping, QSM) in key brainstem areas.
medulla oblongata
pons
especially in the raphe nuclei and reticular formation - core hubs for breathing and autonomic control.
What does that mean?
Higher magnetic susceptibility usually reflects iron accumulation, microglial activation, or loss of myelin - all signs of neuroinflammation.
These changes weren’t random - they tracked with how severe the original infection was.