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
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/
👉 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:
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/