Long COVID in children is often reduced to fatigue.
This study shows something far more concrete - measurable impairment in language skills - speaking, listening, and readingđź§µ
Study design.
N = 1,244 children (ages 3–18) in Hong Kong.
Three groups. 1. long COVID 2. COVID, fully recovered 3. never infected
Language was assessed using LEAP-Q, covering
speaking, listening, reading, writing - in two languages (Chinese + English).
Main finding.
Children with long COVID had significantly lower overall language proficiency than both recovered children and never-infected peers.
Crucial detail.
There was no significant difference between COVID without long COVID and no-COVID groups.
This directly challenges the claim that deficits are just due to lockdowns, masks, school disruption etc
Which domains were most affected?
The largest drops were in speaking and listening.
Reading was also reduced.
Writing showed less consistent differences.
Age matters.
No clear effect in kindergarten.
Clear deficits in primary school.
Strongest impact in secondary school students
Why this makes sense?
Older students are in the reading to learn phase. Language becomes the tool for complex thinking.
COVID often affects attention, working memory, and cognitive endurance - language performance suffers first.
Important nuance.
The negative effect appeared in both the first language and English.
This was not just missed school English, but a broader cognitive impact.
Limitations (fairly stated)
No pre-infection baseline testing.
Parent-reported measures (not clinical language tests).
Cross-sectional design.
Still, the pattern is consistent and developmentally plausible.
What this shows in real life?
Long COVID in children is not subjective or trivial.
It can mean measurable disruption of communication, learning, and daily functioning.
Estimated Long COVID prevalence in children (RECOVER / JAMA)?
Using the stricter PASC-probable definition
Ages 6–11 ~20%
Ages 12–17 ~14%
These are not marginal numbers!
And in the United States?
ACT scores were stable for ~30 years.
After 2019, the composite score drops sharply - to the lowest level in decades.
The decline is synchronous across math, reading, English, and science. And persists.
This is not normal fluctuation.
At the same time, high school GPAs rise or remain stable while ACT scores fall.
That divergence matters - grades adapt, standardized tests don’t.
What’s declining is measured cognitive performance, not just grading standards.
Most countries lack national screening for pediatric long COVID.
Education and healthcare remain siloed.
Recognizing a biological driver would imply responsibility, cost, and abandoning the claim that children are fine.
Instead, the focus stays on learning loss and pandemic disruption -
not on population-level biological burden.
If public health continues to say children are fine,
it is effectively accepting loss of learning, function, and quality of life in a substantial fraction of a generation. @szupraha @msmtcr @ZdravkoOnline @adamkova_vera @adamvojtech86 @RobertPlaga
A public health call to action.
Stop treating pediatric long COVID as a taboo
monitor cognitive and language outcomes in schools
fund pediatric research and diagnostics
and
most importantly - reduce repeated infections as a preventable risk!
Xu at al., The Impact of Long COVID on Language Proficiency Across Different School Levels in Hong Kong. mdpi.com/2076-328X/15/4…
• • •
Missing some Tweet in this thread? You can try to
force a refresh
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 comorbiditiesđź§µ
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.
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..đź§µ
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 brainđź§µ
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.
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)