Vipin M. Vashishtha Profile picture
Dec 27, 2024 10 tweets 4 min read Read on X
COVID pregnancies may have boosted autism risk!

A NEW study shows the onset of autism in COVID exposed babies at 28 months. Researchers found 23 of 211 children (11%), screened positive for autism spectrum disorder, compared with an expected prevalence of 1-2% at that age 1/ Image
When researchers analyzed videos of children lying on their backs in what’s called General Movement Assessment, 14% of infants showed signs of developmental problems. The test evaluates early motor functions & is often used to assess the risk of neurodevelopmental disorders 2/ Image
Later, the findings proved equally troubling. At 6-8 months old, 13 of 109 infants born to infected mothers — almost 12% — had failed to reach developmental milestones. In stark contrast, all infants in a control group born before the pandemic showed normal development. 3/
Around 11.6% of toddlers born to mothers with lab-confirmed SARS-CoV-2 infection during pregnancy showed cognitive, motor or language problems indicative of neurodevelopmental delays. By comparison, only two of 128 unexposed controls — 1.6% — showed such issues. 4/ Image
When the eldest of the COVID-exposed babies reached 28 months, the study found another concerning pattern: 23 of 211 children — almost 11% — screened positive for autism spectrum disorder. 5/
The later findings, currently undergoing peer review ahead of publication, are a reminder that COVID’s long-term consequences, including higher risks for dementia and heart disease, continue to unravel almost five years after the pandemic began. 6/. Image
While the virus is generally known to cause more severe symptoms in adults than in children, emerging data suggest that babies exposed to COVID in utero face elevated risks for preterm birth, congenital heart abnormalities & rare conditions, such as situs inversus. 7/ Image
Children born during the Covid era are now reaching the average age for autism diagnoses. Identifying developmental issues early can open the door to speech and behavioral therapies, which are proven to support a child’s development. 8/ Image
Scientists say the full consequences of in utero exposure to the SARs-CoV-2 may take decades to uncover and understand. Even if a link is established, genetics are likely to play a crucial role. 9/ Image
The researchers continue to analyze stored blood & other specimens from the babies in their study. “It’s a new pathogen. We don’t know how it behaves. Things might appear down the road that we were not expecting.” 10/10

bloomberg.com/news/articles/…

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More from @vipintukur

May 12
#LongCOVID is increasingly emerging as an immune-mediated disorder driven by:

➡️ Viral persistence
➡️ Chronic inflammation
➡️ Immune dysregulation
➡️ Tissue remodeling

👉 The lungs may remain biologically altered long after acute infection resolves. 1/ Image
A new review highlights how persistent immune activation in LongCOVID may lead to:
• Fibrosis-like lung changes
• Endothelial dysfunction
• Microvascular injury
• Ongoing respiratory symptoms

COVID may end clinically—but not biologically.
#LongCOVID #Pulmonology 2/ Image
LongCOVID respiratory sequelae may result from a “perfect storm” of:

➡️ Aberrant immune signaling
➡️ Residual viral antigens
➡️ Microvascular dysfunction
➡️ Dysregulated tissue repair

👉 A unifying pathophysiology is slowly taking shape. 3/ Image
Read 9 tweets
Apr 22
COVID-19 may be, in part, a mitochondrial disease.

➡️ A Cambridge review shows SARS-CoV-2 disrupts mitochondrial function in lung cells—driving inflammation and worsening pneumonia.

➡️ Emerging studies suggest even after the active infection is resolved, residual viral proteins, particularly SARS-CoV-2 spike protein, may linger and continue to cause damage to the mitochondria by increasing oxidative stress and disrupting energy metabolism, offering a plausible mechanism for #LongCOVID. 1/

H/T: @CatchTheBabyImage
COVID-19 is not just viral—it’s metabolic.

SARS-CoV-2 hijacks mitochondria →
↓ Energy production
↑ Inflammatory signaling

A key pathway worsening lung injury. 2/ Image
Mitochondria may link acute COVID → #LongCOVID.

Viral disruption of mitochondrial function can persist, sustaining oxidative stress and immune dysregulation even after infection. 3/ Image
Read 5 tweets
Apr 16
How does COVID affect the brain?

➡️ New research highlights a key player: astrocytes—the brain’s support cells.

👉 SARS-CoV-2 can disrupt their function, with downstream effects on neurons. 1/ Image
Key mechanism:

➡️ The virus can infect or impair astrocytes, which normally:

• Support neurons
• Regulate metabolism
• Maintain brain homeostasis

➡️ Disruption → neuronal dysfunction 2/ Image
What happens next?

➡️ Altered astrocytes can:

• Trigger inflammation
• Impair energy supply to neurons
• Contribute to neuronal injury or death 3/ Image
Read 6 tweets
Apr 10
New study shows SARS-CoV-2 directly damages heart cell mitochondria—key energy engines—offering a mechanistic link to #LongCOVID cardiovascular symptoms. 1/ Image
#LongCOVID may be a mitochondrial disease: electron microscopy reveals structural damage & myofilament breakdown in cardiomyocytes. 2/ Image
Biopsies from LongCOVID patients confirm myocarditis with mitochondrial disruption—mirrored in infected animal models. Strong biological plausibility for persistent cardiac symptoms. 3/ Image
Read 5 tweets
Mar 24
Autoantibodies as drivers of #LongCOVID

➡️ Compelling new evidence strengthens the autoimmune hypothesis of long COVID.

Transfer of patient-derived IgG induces pain-associated behaviours in mice—suggesting a causal, not associative, role.

Key experiment:

➡️ Total IgG from long COVID patients → injected into mice

➡️ Result: mechanical hypersensitivity (allodynia)

This recapitulates a core clinical feature—chronic pain.

➡️ Strikingly, pathogenicity is durable:
IgG collected 2 years later from persistently symptomatic patients
→ still induces pain in vivo

Implies long-term stability of autoreactive clones. 1/Image
Not all LongCOVID is the same.

➡️ Patients stratified using:
• GFAP
• Neurofilament light chain (NFL)
• IFN-β

➡️ Distinct biomarker-defined subgroups with different pathogenic pathways.

Proteome-wide profiling reveals:

➡️ Subgroup-specific autoantibody signatures
➡️ Persistent over time
➡️ Independently validated

Supports biological heterogeneity rather than a single syndrome. 2/Image
Conceptually aligns with conditions like fibromyalgia:

👉 Chronic symptoms driven by functional autoantibodies
👉 Neuro-immune interface involvement

➡️ Clinical implications:

• Identifying pathogenic IgG could enable risk stratification
• Opens avenues for targeted immunomodulation (e.g., IVIG, plasmapheresis, B-cell therapies?)

➡️ Methodological strength:

-Functional transfer model (human → mouse)
-Longitudinal sampling
-Multi-omics support

➡️ Moves the field from correlation → causation. 3/Image
Image
Read 4 tweets
Mar 13
New research finds that SARS-CoV-2 spike protein can persist in the gut of people with #LongCOVID, even months after infection.

➡️ This persistent viral antigen may drive ongoing immune changes in intestinal tissue.

➡️ Scientists detected viral spike RNA and protein in colon and ileum biopsies from Long COVID patients.

➡️ In these regions, genes linked to inflammation, immune dysfunction, and tissue stress were altered. 1/Image
Persistent spike-positive areas in the colon showed increased immune cell activity, including:

• Macrophages
• Plasma cells
• Regulatory T cells

Suggesting an active local immune response in the gut.

➡️ Researchers also found disrupted expression of key immune-signaling genes, indicating impaired immune coordination and chronic inflammation in gut tissues. 2/Image
SARS-CoV-2 persistence is a proposed driver of Long COVID (LC), but the in-situ relationship between residual viral antigen and immune dysregulation remains poorly defined.

➡️ This NEW study provides robust evidence that persistent SARS-CoV-2 Spike protein detection in the gut is not immunologically inert.

➡️ Instead, it is actively associated with distinct, immune cell composition shifts and a dysfunctional pro-inflammatory transcriptional profile, supporting the hypothesis that retained viral antigen drives chronic immune dysregulation in tissue of LongCOVID subjects. 3/Image
Read 4 tweets

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