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/
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/
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/
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/.
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/
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/
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/
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
👉 The lungs may remain biologically altered long after acute infection resolves. 1/
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/
LongCOVID respiratory sequelae may result from a “perfect storm” of:
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: @CatchTheBaby
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/
Mitochondria may link acute COVID → #LongCOVID.
Viral disruption of mitochondrial function can persist, sustaining oxidative stress and immune dysregulation even after infection. 3/
New study shows SARS-CoV-2 directly damages heart cell mitochondria—key energy engines—offering a mechanistic link to #LongCOVID cardiovascular symptoms. 1/
#LongCOVID may be a mitochondrial disease: electron microscopy reveals structural damage & myofilament breakdown in cardiomyocytes. 2/
Biopsies from LongCOVID patients confirm myocarditis with mitochondrial disruption—mirrored in infected animal models. Strong biological plausibility for persistent cardiac symptoms. 3/
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/
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/
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/