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Vipin M. Vashishtha Profile picture
@vipintukur
Jun 2, 2025 • 7 tweets • 3 min read • Read on X
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Globally, NB.1.8.1 is now the dominant variant. The WHO has issued a warning about rising COVID-19 activity in the Western Pacific, Southeast Asia, and Eastern Mediterranean, driven by NB.1.8.1 this week.

H/T: @RajlabN Image
Classified as a "variant under monitoring" by the WHO & “ Nimbus” by @TRyanGregory, NB.1.8.1 has triggered a seventh consecutive week of surges in Southeast Asia. Taiwan has seen ER visits double again this week. 2/

focustaiwan.tw/society/202505…
@TRyanGregory China is reporting widespread infections with NB.1.8.1 causing severe throat pain described as “razor blade throat.”

However, the #Nimbus aka NB.1.8.1 wave in Hong Kong and Singapore may have peaked. 3/ Image
@TRyanGregory A new surge is going on in India too. Still early days…active Covid-19 cases have risen to 3,758, with Kerala reporting the highest at 1,400 cases.

One death is also reported from my own district though no uptick is noticed in children so far. 4/4

indtoday.com/covid-19-cases…Image
@TRyanGregory And what about vaccines?

The FDA has recommended updating Fall 2025 COVID vaccines to target LP.8.1 which is the dominant variant in the United States now.

But, LP.8.1 is fairly different from NB.1.8.1 which is the dominant variant worldwide. 5/

nbcnews.com/news/amp/rcna2…
@TRyanGregory Last year’s Fall 2024 COVID vaccine targeted KP.2 for Moderna/Pfizer & JN.1 for Novavax. Although FDA’s advisory panel favored sticking with JN.1-based strains for Fall 2025, they agreed LP.8.1 is an appropriate alternative for 2025/2026 season 6/

fda.gov/media/186567/d…Image
@TRyanGregory And what about India?

No JN.1/adapted booster
The only Omicron-adapted vax is Gemcovac-OM based on BA.1
Even this isn’t freely available
The only category who need boosters in India: elderly w/ comorbidities or immunocompromised

So what’s the recs for Covid vax here👇 7/7 Image

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More from @vipintukur

Vipin M. Vashishtha Profile picture
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
Vipin M. Vashishtha Profile picture
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
Vipin M. Vashishtha Profile picture
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
Vipin M. Vashishtha Profile picture
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
Vipin M. Vashishtha Profile picture
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
Vipin M. Vashishtha Profile picture
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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