Zdenek Vrozina Profile picture
Nov 5 13 tweets 3 min read Read on X
A new study in The Lancet Child & Adolescent Health followed nearly 14 million children in England.
It shows that SARS-CoV-2 infection leaves long-term marks on the vascular and immune system - even in kids.
Not just for weeks, but measurable up to a year later🧵
After COVID-19, children had a sharply increased risk of
systemic inflammatory syndromes (MIS-C, etc)
venous thrombosis
thrombocytopenia
myocarditis and pericarditis
And part of these risks remained elevated 12 months post-infection.
That means - even if a child feels fine after COVID, the body may stay in a dysregulated immune and vascular state - with lingering inflammation and endothelial stress.
In biological terms, COVID leaves a footprint
Mechanisms are consistent with what we see in adults
endothelial injury,
microcirculatory dysfunction,
coagulation changes,
viral antigen persistence.
Together, they explain why a mild infection doesn’t always mean a harmless one.
This study covers Jan 2020 - Mar 2022, ie mainly the Alpha and Delta waves.
That’s key - those variants triggered the strongest vascular and inflammatory responses.
Omicron infections were only starting to appear by the end of the study window.
But newer data are in.
A Nature Communications 2025 study following children and adolescents in the Omicron era confirms that infection still carries measurable cardiovascular risks - even now.
Researchers found higher post-COVID rates of
hypertension
arrhythmias
myocarditis
venous thrombosis
and even cardiomyopathy or heart failure
- compared to non-infected peers, regardless of initial severity.
So
Delta left stronger, more obvious sequelae.
Omicron looks milder acutely, but it’s not biologically neutral.
In a fraction of children, the infection still leaves a detectable vascular and immune imprint.
In kids, COVID rarely looks dramatic - but it doesn’t vanish without a trace.
The virus leaves subtle, measurable effects on vessels, the heart, and immunity.
Mild ≠ harmless.
Preventing infection is important.
Public health failed to recognize that not hospitalized ≠ unaffected.
Kids deserve protection not only from death, but from the silent biology that shapes their future health. @szupraha @ZdravkoOnline @adamvojtech86
Even when symptoms fade, biology doesn’t always reset.
Endothelial scars, immune shifts, and metabolic traces can persist - shaping long-term health in ways we’re only beginning to map.
Sampri at al., Vascular and inflammatory diseases after COVID-19 infection and vaccination in children and young people in England: a retrospective, population-based cohort study using linked electronic health records. Child & Adolescent Health 2025. thelancet.com/journals/lanch…
Zhang at al., Cardiovascular post-acute sequelae of SARS-CoV-2 in children and adolescents: cohort study using electronic health records. Nature Communications 2025. nature.com/articles/s4146…

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Zdenek Vrozina

Zdenek Vrozina Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @ZdenekVrozina

Nov 4
New study in BMC Immunology shows that COVID-19 leaves a lasting “aka Long Covid” imprint in the immune cells of older adults. What does that mean - and why does it matter?🧵
Months after recovery, immune cells in elderly people remain abnormally prone to die - through apoptosis.
Even when the virus is long gone, the immune system still shows signs of cellular damage and exhaustion.
Researchers analyzed peripheral blood mononuclear cells (PBMCs) - the core soldiers of the immune system, including T cells and monocytes.
In post-COVID seniors, twice as many cells were apoptotic compared to healthy controls.
Read 18 tweets
Nov 3
A experimental study in Scientific Reports shows that the SARS-CoV-2 spike protein alone can trigger an autoimmune response against the ACE2 receptor - the very receptor the virus uses to enter cells.
The mechanism mirrors tissue damage seen in severe COVID-19🧵
This study is a proof-of-concept.
When the immune system reacts to the SARS-CoV-2 spike protein, part of that response can flip into autoimmunity against ACE2, the receptor the virus normally uses to enter cells.
In other words - the immune system doesn’t just make antibodies against the spike -
it can also generate anti-idiotype antibodies (and T-cell clones) that mistakenly recognize and attack ACE2, because ACE2 structurally mirrors the very site the spike protein binds to.
Read 19 tweets
Nov 3
A massive Swedish study on Nature Communications Medicine tracked 810,851 people after COVID.
Only 1.4% received an official post-COVID-19 condition (PCC) diagnosis - but that reflects only those who made it into the system.
Real prevalence of long COVID is many times higher🧵
Who was most likely to be diagnosed with PCC?
severe acute infection
unvaccinated status
female sex, older age
higher education, essential jobs (healthcare, teachers, drivers…)
pre-existing conditions - asthma, thrombosis, fibromyalgia, depression, anxiety, stress disorders
Biological core of the findings
Severity of acute infection
The strongest predictor by far.
The more severe the acute phase, the higher the PCC risk - stronger inflammation, higher viral load, and deeper tissue injury mean a greater chance some immune processes remain stuck on.
Read 13 tweets
Nov 2
While COVID-19 (Omicron) in children is often called mild, new evidence shows a darker side.
For a small fraction who develop brain inflammation, it becomes a deadly and disabling lottery.
The Lottery of Consequences🧵
A new multicenter study in Pediatric Neurology followed 102 children with COVID-19 related encephalopathy or encephalitis.
The outcome?
Half of them either died or were left severely disabled.
In pediatric ICUs, mortality reached 26.5%.
Among survivors, 35% left the hospital with severe neurological impairment - movement, speech, cognition, seizures.
And one year later?
No improvement.
Those who left disabled stayed disabled.
Read 10 tweets
Nov 1
A new paper in Pathogens makes a bold claim:
Aging, HIV, and Long COVID - three very different conditions - might share a common root cause - mitochondrial dysfunction.
Different paths, same destination🧵
The authors see mitochondria not as cellular batteries only, but as conductors of life.
When their rhythm falters, the whole orchestra follows - energy drops, immunity weakens, repair fails.
That’s the hidden thread connecting aging, HIV, and Long COVID.
Across all three, the same sequence unfolds.
Excess ROS
Impaired mitophagy (PINK1–Parkin failure)
Loss of biogenesis (↓ PGC-1)
Persistent inflammation via cGAS-STING
Cells survive - but stop functioning properly.
Read 12 tweets
Oct 31
New study in Journal of Neuroinflammation, 2025, reveals how the SARS-CoV-2 spike protein alone - without the whole virus - can trigger inflammation and cellular aging in human brain cells - astrocytes.
The key - activation of the innate immune receptor TLR7.🧵
The spike’s S1 subunit enters astrocytes and accumulates in endolysosomes - the cell’s recycling centers.
Inside, it causes loss of acidity, membrane damage, and enzyme leakage (galectin-3, cathepsin B).
Result - inflammatory signaling and cellular senescence begin.
A tiny sequence in spike - the multibasic motif RRAR - is crucial.
When researchers deleted it, there was no damage and no senescence.
That same motif is also what makes SARS-CoV-2 highly infectious.
Importantly, the vaccine-derived spike also contains this RRAR motif - the same sequence identified here as essential for the toxic effect on astrocytes.
Read 14 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(