Another study adds to growing evidence:
Children exposed in utero to maternal COVID-19 face a higher risk of neurodevelopmental issues by age 3.
It’s part of a broader pattern showing how SARS-CoV-2 can leave long biological traces - even before birth🧵
Study in Obstetrics & Gynecology, 2025
18,124 births (Mass General Brigham, 2020-2021).
861 mothers had confirmed SARS-CoV-2 infection during pregnancy.
By age 3, 16.3% of exposed children had a neurodevelopmental diagnosis vs 9.7% of unexposed.
After adjustment for age, race, insurance, and preterm birth:
+29% higher risk overall.
Biggest effects
infection in the third trimester
male offspring
The virus triggers maternal immune activation, inflammation, and changes in placental blood flow - all of which can subtly reshape brain development, especially late in pregnancy when key neural circuits are wiring up.
Most exposed children develop normally.
But at the population level, that 6-7 additional cases per 100 exposed births is not trivial.
It’s a measurable, biologically plausible signal - not noise.
Male fetuses seem more vulnerable.
Their brains have weaker anti-inflammatory buffering and less stable microglial regulation.
This sex-specific sensitivity is seen across other prenatal stress and infection models too.
Similar findings are emerging from other cohorts - in the U.S., Israel, Denmark, Italy.
Different settings, same message:
prenatal SARS-CoV-2 exposure - higher odds of speech, motor, or social developmental delays.
It fits a bigger truth.
SARS-CoV-2 is not just a respiratory virus.
It disrupts immune, vascular, and developmental systems - including those that shape the brain before birth.
The authors call for long-term neurodevelopmental follow-up of pandemic-era children, especially boys and those exposed in late pregnancy.
It’s a reasonable - and urgent - precaution.
Each new study reinforces what should already be obvious -
protecting pregnant people from infection isn’t only about them - it’s about the next generation’s brain health. @szupraha @ZdravkoOnline @adamvojtech86
That’s the quiet tragedy behind studies like this.
For years, public health messaging has focused on mildness, while avoiding the harder truth - that infection during pregnancy can have lasting effects on the child.
It’s not about panic. It’s about honesty and prevention.
Inform pregnant people clearly.
Support measures to reduce infection risk.
Ensure long-term follow-up for exposed children.
Silence doesn’t protect anyone - it only erases accountability.
Shook et al. Neurodevelopmental Outcomes of 3-Year-Old Children Exposed to Maternal SARS-CoV-2 Infection in Utero.
Obstetrics & Gynecology. Oct 30, 2025. journals.lww.com/greenjournal/f…
Public health had sufficient signals of varying quality from earlier studies.
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.
MRI alone may not be enough to rule out post-COVID heart inflammation.
A new JACC 2025 study found that even young, previously healthy adults with normal ECG, echo, and MRI can have microscopic heart damage - inflammation, microvascular damage, and cell necrosis.🧵
The study evaluated 423 long-COVID patients with persistent chest pain.
Most had normal or near-normal cardiac MRI, with only subtle changes in strain or perfusion.
A smaller subgroup (25 patients) whose symptoms persisted despite normal imaging underwent endomyocardial biopsy, revealing -
microangiopathy
necrosis of cardiomyocytes (76%) (!)
fibrotic changes
and in some cases, SARS-CoV-2 N-protein still present in cardiac tissue.
A new Russian review in IJMS shows how SARS-CoV-2 reshapes the epigenome - weaving together known mechanisms into something deeper.
It’s not just long COVID.
It’s a virus that rewrites the factory that makes immune cells - the bone marrow🧵
Zolotarenko puts special emphasis on this point.
The changes don’t appear in mature immune cells -
they start in their progenitors.
These hematopoietic precursors are born misprogrammed inside the marrow.
That’s why, even after infection clears, the body keeps producing confused immune cells.
The virus is gone, but its instructions remain.
An epigenetic imprint continues to guide new cells months later.
A new important study in Frontiers in Immunology shows that repeated SARS-CoV-2 infections are beginning to display the same patterns seen in chronic viral infections - narrowing of the T-cell repertoire, exhaustion, and loss of immune flexibility (!)🧵
The immune repertoire doesn’t fully recover after infection. Diversity shrinks, and with reinfection the system no longer returns to balance.
The study analyzed T-cell receptors in people after a first infection and after reinfection with SARS-CoV-2.
The result?
Reinfection isn’t just another infection - it leaves a measurable imprint on the immune system.
A study from Krakow followed hospitalized COVID-19 patients for five years to see if their initial immune profiles - T, B, and NK cells - could predict who would
die in the following years, or develop long COVID.🧵
Out of 103 patients from 2020, researchers followed 80 over 54 months.
23 had died, 57 were alive - and about half of those survivors (29 people) still lived with long COVID symptoms.
That’s one of the longest immune follow-ups after COVID-19 so far.
During the acute infection, those with severe disease showed a collapse of T and NK cells.
Their total T cells dropped to a median of 340 per µl (vs 705 in milder cases).
CD4+ helper T cells fell to 183 vs 452, and CD8+ cytotoxic T cells to 109 vs 227.
Even NK cells were lower (107 vs 157).
Meanwhile, the proportion of B cells was paradoxically higher - 18.5% vs 12.5%.
A new preprint from Aarhus University shows something striking:
people with post-COVID, MCS, and functional disorders all share the same brain pattern -
split hemispheres, weakened bridges between left and right (!),
overloaded smell and sensory circuits🧵
The study scanned 57 women (post-COVID, MCS, FSD, controls) using diffusion MRI (DTI).
It didn’t measure brain activity, but rather its wiring - the white-matter highways that carry information between regions.
Result.
Interhemispheric connectivity - the bridge between left and right hemispheres - was reduced by 70% in all three patient groups.
That means information flow across the brain is slower, less coordinated, and less efficient.