Post

@TheLancet

@DavidLVBauer

More from @vipintukur

Vipin M. Vashishtha

@vipintukur

May 17

SARS-CoV-2 spike protein may directly amplify brain inflammation.

➡️ Researchers found that spike proteins can colocalize with amyloid-β (Aβ) and trigger distinct inflammatory responses in microglia — the brain’s immune cells.

➡️ This raises important questions about potential long-term neurodegenerative consequences of COVID-19. 1/

Researchers developed advanced “expansion microscopy” techniques that physically enlarge human brain tissue, allowing scientists to see disease-related structures at near-nanoscale resolution using ordinary microscopes. 2/

Applying this method to brains from some COVID-19 patients revealed tiny amyloid-like protein clusters closely associated with SARS-CoV-2 particles in a small subset of cases, suggesting a possible link between COVID-19, neuroinflammation, and abnormal protein aggregation in the brain.

The study highlights how ultra-high-resolution imaging could uncover previously hidden mechanisms of neurological disease. 3/

Read 4 tweets

Vipin M. Vashishtha

@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/

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:

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

👉 A unifying pathophysiology is slowly taking shape. 3/

Read 9 tweets

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

Share this page!

Enter URL or ID to Unroll

Vipin M. Vashishtha

Try unrolling a thread yourself!

More from @vipintukur

Vipin M. Vashishtha

Vipin M. Vashishtha

Vipin M. Vashishtha

Vipin M. Vashishtha

Vipin M. Vashishtha

Vipin M. Vashishtha

Did Thread Reader help you today?

Don't want to be a Premium member but still want to support us?

Send Email!