Vipin M. Vashishtha Profile picture
Sep 26, 2024 8 tweets 3 min read Read on X
A NEW nasal spray that trap & neutralize not only SARS-CoV-2, Influenza, RSV, Adeno & many other viruses & bacteria that are inhaled into the nose, immobilizing them until they die. The substance is >99.9% effective & contains no drugs 1/ Image
The FDA approved substance in the spray is known as the Pathogen Capture and Neutralizing Spray (PCANS), & contains no drugs of any kind.
Instead, the spray forms a gel that lines the inside of the nose. 2/ Image
While this gel doesn't affect the user's breathing, it does trap any viruses or bacteria that are subsequently inhaled into the nose, immobilizing them until they die. 3/ Image
In lab tests, the spray protected mice from a mouse-adapted form of the H1N1 influenza virus, even when that virus was administered at 25 times the lethal dose. 4/ Image
What's more, virus levels in the animals' lungs were reduced by over 99.99% as compared to an untreated control group of mice. The spray was retained in the rodents' noses for up to eight hours, and was effective at blocking infection for at least four hours. 5/
Although PCANS has yet to be tested on humans, it has been used in a 3D-printed model of a human nose, where it captured twice as many microbe-containing droplets as mucus alone. 6/ Image
It blocked and neutralized almost 100% of all viruses and bacteria we tested, including influenza, SARS-CoV-2, RSV, adenovirus, K Pneumonia and more. 7/
And if you suffer from allergies, take note – the researchers believe the spray could one day also be used on a daily basis to trap and neutralize allergens. 8/8

onlinelibrary.wiley.com/doi/10.1002/ad…

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More from @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: @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
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/Image
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/ Image
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/ Image
Read 4 tweets

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