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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This study does not tell us what exactly causes long COVID or ME/CFS, nor does it test clinical symptoms like PEM.
But it may tell us something just as important - what type of biological problem this likely is..🧵
The authors isolated immunoglobulins (IgG) from people with post-infectious ME/CFS, including post-COVID ME/CFS, and tested what these antibodies do to healthy cells.
In a subset of patients, these IgG alter the behavior of endothelial cells and their mitochondria.
Not by killing the cells or shutting down ATP production.
This isn’t a new comparison.
For years, parallels between NeuroHIV and neuro-COVID/Long COVID have been discussed across fields.
What’s new is that they are now formally described as shared CNS mechanisms, not just analogy!🧵
Just a few years ago, parallels like
HIV - SARS-CoV-2
HAND - brain fog/neuro-LC
microglia - chronic inflammation
vasculature - cognition
were treated mainly as interesting analogies. With caution not to overstate them.
This new review formalizes the shift. These parallels are not Twitter pattern recognition, but convergent CNS phenotypes following viral insults.
A new review shows they are biologically grounded similarities.
A new review links Alzheimer’s disease, Parkinson’s disease, and COVID-19 through a shared core - neuroinflammation + oxidative stress.
The same pathways, the same immune nodes, the same vulnerabilities of the brain🧵
Key players.
Microglia (the brain’s innate immune cells) and neutrophils (peripheral rapid responders).
When the blood–brain barrier (BBB) is disrupted, neutrophils enter the CNS and inflammation becomes self-amplifying.
Neutrophils can form NETs (neutrophil extracellular traps - DNA + histones + enzymes like MPO/elastase).
In the brain, NETs mean oxidative damage, mitochondrial stress, neuronal injury - and further microglial activation. A vicious cycle.
Long COVID in children is often reduced to fatigue.
This study shows something far more concrete - measurable impairment in language skills - speaking, listening, and reading🧵
A new single-cell multiome study helps answer a key long-COVID question.
Where do the pathological monocyte programs seen later actually come from?
This paper maps how classical monocytes change already during the acute phase of COVID-19.
Using paired RNA + chromatin profiling, the authors analyze immune cells across disease severity from healthy controls to critical COVID.
A clear pattern emerges -
myeloid cells, especially classical monocytes, carry much of the severity-associated signal.
The choroid plexus (ChP) has become one of the most consistent findings in post-COVID and long COVID neuroimaging.
It is enlarged.
But larger alone doesn’t yet tell us what is actually happening🧵
A new paper in Alzheimer’s & Dementia moves the ChP story one step further.
It’s no longer just about volume - the authors also measure choroid plexus blood flow (CBF) and link it to cognition and biomarkers.
Study design.
86 long COVID patients, 67 recovered COVID, 26 healthy controls.
MRI + pCASL perfusion imaging.
In a subset of long COVID patients, blood biomarkers (GFAP, p-tau217, etc)