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/
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/
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/
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/
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/
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
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/