Zdenek Vrozina Profile picture
Feb 6 9 tweets 2 min read Read on X
If normal population plasma truly carries more low-grade inflammation, this study hints at a fork in the road.
Either we lower the bar and call it a new normal,
or this is a hidden population burden that will surface later as comorbidities🧵
A new study on the cytokine IL-32 after COVID-19 points directly at this uncomfortable question.
The authors analyzed nearly 1,000 healthy blood donors sampled before and during the pandemic, plus 212 hospitalized COVID-19 patients.
The result is consistent - plasma collected after 2020 shows systematically higher IL-32 levels compared to pre-pandemic plasma.
Importantly -
this is seen even in people without severe COVID,
the authors interpret it as a consequence of mass exposure to SARS-CoV-2,
suggesting a persistent, low-grade inflammatory imprint at the population level.
What this does not mean?
No contamination, no acute inflammation or infectious risk, no loss of transfusion safety.
What it does mean?
The reference normal of plasma may have shifted since 2019,
some cytokines (here IL-32) behave like long-term memory of immune activation,
in simple words - plasma is no longer immunologically identical to the pre-pandemic era, even in clinically healthy people.
A key detail.
IL-32 is not a cytokine storm marker.
It reflects chronic, silent inflammation/immune reprogramming.
That’s exactly why this finding matters.
The question isn’t whether this matters. If population baseline inflammation has shifted, this affects how we interpret biomarkers, controls, reference ranges, and biobank data going forward.
Miano et al., Frontiers in Immunology, 2026. Association of SARS-CoV-2 infection with long-lasting increase in circulating IL-32 levels. frontiersin.org/journals/immun…

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More from @ZdenekVrozina

May 8
A new study in Frontiers in Cardiovascular Medicine looked at a very important question.
Can a history of COVID-19 be linked to impaired coronary blood flow, even when the main coronary arteries look normal?🧵
The authors included 190 patients with unstable angina and normal coronary arteries.
Half of them had a confirmed history of COVID-19.
The other half did not.
The key difference between the two groups was previous COVID infection.
The result was striking.
Patients with prior COVID-19 had a much higher rate of coronary slow flow.
COVID+ group 18.9%
COVID− group 5.3%
That is more than a threefold difference.
Read 21 tweets
May 7
Why do some people develop life-threatening viral disease, while others clear the same virus with only mild symptoms?
One answer is becoming clearer.
In some people, the first line of antiviral defense is already weakened before the virus arrives🧵
That first line is type I interferon.
Type I - especially IFN-α and IFN-ω - act like an early alarm system. When a virus enters the body, they help cells switch into an antiviral state before the infection spreads too far.
A landmark study from the Casanova lab found that some patients with life-threatening COVID-19 had autoantibodies that neutralized type I interferons.
In that cohort, these neutralizing autoantibodies were found in about 10% of critical COVID-19 cases.
Read 16 tweets
May 5
A new JAMA Neurology meta analysis on pure autonomic failure (PAF) is highly relevant to the broader discussion around POTS, long COVID dysautonomia, and early neurodegeneration.
Not because PAF is the same as POTS.
It is not. But…🧵@DavidJoffe64
It is important because it shows what can be learned when an autonomic syndrome is carefully defined and followed over time.
PAF is a form of autonomic failure, usually marked by neurogenic orthostatic hypotension.
In simple terms. When a person stands up, blood pressure drops, and the autonomic nervous system fails to compensate properly.
That is very different from simply feeling dizzy on standing.
Read 23 tweets
May 4
A new PECOS study followed children and young people after SARS-CoV-2 infection and compared them with uninfected controls.
The question was simple - do post COVID symptoms in kids fade over the first year?
The answer - not really.
The study included 852 participants aged 0-21.
705 had confirmed SARS-CoV-2 infection
147 were uninfected controls
Among the infected group, 558 completed the 12 month follow-up.
At baseline, about two-thirds of infected participants reported at least one symptom after recovery from their initial infection!
That is roughly 470 out of 705 children and young people.
So this was not a tiny subgroup with rare complaints.
Read 17 tweets
May 3
A new large cohort study in Frontiers in Medicine looked at people who developed shingles after COVID-19.
Could shingles after COVID be more than just a painful rash - with possible links to later blood-cancer risk?🧵
The authors used the TriNetX global health network - electronic health records from more than 140 healthcare organizations.
They compared COVID-19 survivors who developed shingles within 1 year with COVID-19 survivors who did not.
After matching, the study compared roughly 29,270 people in each group.
The follow-up 3 years.
The authors were not only looking at short-term symptoms, but later infectious and blood-related outcomes.
Read 14 tweets
Apr 29
A new narrative review in Communications Medicine sums up where the field stands on long COVID.
Not as one single, uniform diagnosis, but as a complex, multisystem condition after SARS2 infection🧵
Its value is in the synthesis. It brings together immunology, neurology, vascular biology, metabolism, and clinical medicine into one framework.
The review covers prevalence, pathophysiology, biomarkers, treatment strategies, and future research directions. It is a broad interpretation of the current literature.
Read 21 tweets

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