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…
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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)
CD14 monocytes as the main pathological driver of long COVID?
A new Nature Immunology paper points to a clear biological signal in long COVID - CD14 monocytes - cells of the innate immune systemđź§µ
The authors combined
single-cell RNA-seq
ATAC-seq (epigenetics)
plasma cytokines
functional stimulation assays
bronchoalveolar lavage (lung immune cells)
Crucially, they stratified patients by acute COVID severity - something many studies fail to do.
The central finding.
A distinct pathological monocytic program called LC-Mo
(long COVID monocyte state).
Not ongoing activation.
It’s a stable switch into a different cellular mode.
ME/CFS is sometimes framed as a body locked in stress mode.
The sympathetic nervous system permanently switched on.
Fight-or-flight with no way out.
It made sense.
Almost too much senseđź§µ
But the data have started telling a different story.
Not of a system that’s too strong -
but of one that’s exhausted.
A recent Health Rising analysis puts forward a striking idea -
in ME/CFS, the sympathetic nervous system may be breaking down on two levels at once -
in the brain and in the body.
Not overactive.
Not underactive.
Depleted.
Review paper.
At the center of Long COVID are three processes that reinforce each other -
persistent viral material, damage to the gut barrier, and chronic immune dysregulation. Together, they help explain why neurological and neuropsychiatric symptoms are so common and so persistentđź§µ
Viral persistence.
In a subset of people, fragments of SARS-CoV-2 - especially spike protein - persist for months or even years after the acute infection.
These viral remnants don’t need to actively replicate. Their continued presence is enough to keep the immune system switched on, similar to what we see in chronic viral infections like HIV.
The gut is a key driver.
SARS-CoV-2 infects intestinal epithelial cells, where ACE2 is highly expressed.
This leads to persistent gut dysbiosis, breakdown of epithelial tight junctions, and altered IgA/IgG coating of commensal bacteria - a clear sign of disrupted mucosal immune control.