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Vipin M. Vashishtha

@vipintukur

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: @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/

Read 5 tweets

Vipin M. Vashishtha

@vipintukur

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/

Key mechanism:

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

• Support neurons
• Regulate metabolism
• Maintain brain homeostasis

➡️ Disruption → neuronal dysfunction 2/

What happens next?

➡️ Altered astrocytes can:

• Trigger inflammation
• Impair energy supply to neurons
• Contribute to neuronal injury or death 3/

Read 6 tweets

Vipin M. Vashishtha

@vipintukur

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/

#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/

Read 5 tweets

Vipin M. Vashishtha

@vipintukur

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/

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/

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/

Read 4 tweets

Vipin M. Vashishtha

@vipintukur

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/

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/

Read 4 tweets

Vipin M. Vashishtha

@vipintukur

Mar 10

New research suggests that gut bacteria may contribute to neurological symptoms in #LongCOVID.

➡️ Small particles released by gut microbes—called extracellular vesicles—may trigger inflammation affecting both the body and the brain.

➡️ Scientists found that people with Long COVID and neurological symptoms show a persistent imbalance in gut microbiota.

➡️ This altered microbiome may disrupt the intestinal barrier and promote systemic inflammation. 1/

In experiments, transferring gut microbes from LongCOVID patients into mice caused intestinal barrier damage and signs of brain inflammation.

➡️ This suggests a biological link between the gut and neurological symptoms. 2/

Gut microbe–derived vesicles were shown to activate inflammatory pathways and immune cells, including microglia in the brain.

➡️ These processes may contribute to symptoms such as brain fog. 3/

Read 4 tweets

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