A NEW review of 16 studies found that people who had COVID have smaller brain volumes than controls on scans taken more than 6 weeks after infection and that more severe COVID infections were associated with the most difference in brain volume. 1/
Given the frequency of findings in regions susceptible to inflammation and hypoxia, immune or hypoxia modulated neuroinflammation is a plausible mechanism for brain volume differences after COVID-19. 2/2
A man who had recovered from COVID and tested negative on nasopharyngeal swab was found to have SARS-CoV-2 spike protein in his small intestine, especially in ulcerated areas. 1/
This was associated with increased Vascular Endothelial Growth Factor (VEGF) and Fibronectin expression, as well as structural changes in intercellular junctions between intestinal cells. 2/
SARS-CoV-2 can persist in the gut and cause long-term effects, inducing vascular and epithelial changes, even after it is no longer detected in the nose or throat. 3/
Researchers have pioneered an influenza virus vector-based nasal spray vaccine platform and developed a nasal spray H5N1 avian influenza vaccine. 1/
Genetic surveillance has identified mutations that enhance H5N1's affinity for human upper respiratory cells, raising concerns that further adaptation or recombination with seasonal flu could significantly increase the risk of a pandemic. 2/
Preparation for a potential H5N1 pandemic is urgent, with the U.S. allocating 500 million USD to pharmaceutical companiesfor mRNA-based vaccine development. 3/
Researchers have developed an oral antiviral drug candidate for COVID-19 that could overcome major limitations of Paxlovid, currently the most prescribed oral treatment. 1/
As with its predecessor, the new drug candidate, Jun13296, targets a different viral protein than Paxlovid does and works alone rather than in combination with another drug called ritonavir. 2/
This new compound, #Jun3296 is more potent than the 1st generation candidate. In animal studies, this 2nd-generation inhibitor still provides 90% protection at just one-third dose of the initial compound and significantly outperforms it in reducing viral loads in the lungs. 3/
Even after 5 yrs since its arrival, SARS-CoV-2 mutations keep emerging. A new variant LP.8.1 is rising. Almost 1 in 5 COVID cases in New South Wales are it. In the UK, it accounts for at least 3 in 5 cases. Just what is LP.8.1? Is it worrying? 1/
LP.8.1 was first detected in July 2024. It’s a descendant of Omicron, specifically of KP.1.1.3, which is descended from JN.1, a subvariant that caused large waves of COVID infections around the world in late 2023 and early 2024. 2/
The WHO designated LP.8.1 as a variant under monitoring in January. This was in response to its significant growth globally, and reflects that it has genetic changes which may allow the virus to spread more easily and pose a greater risk to human health. 3/
SARS-CoV-2 spike protein binds fibrinogen, causing thrombo-inflammation, according to a recent study. The virus must bind to fibrinogen, but why? Could this relationship help the virus evolve? Could this cause post-COVID heart attacks? 1/
Scientists often think they grasp a virus's anatomy, tricks, and body movement. But occasionally, we discover something unexpected that radically transforms how we view an infection. 2/
Some strategies are well documented: antigenic drift, glycan shielding, immune suppression. But every so often, we stumble upon a novel mechanism that redefines our understanding of viral pathogenesis. 3/
COVID-19 increases the risk of autoimmune diseases including rheumatoid arthritis and type 1 diabetes. The virus alters the immune system in unknown ways, making it difficult to design medicines to prevent post-COVID autoimmunity. 1/
One leading hypothesis involves viral “molecular mimics”—proteins from the virus that resemble the body’s own proteins. These mimics may trigger an immune response against the virus but unintentionally cause the immune system to target healthy tissues as well. 2/
Thanks to recent advancements in data analysis and machine learning, scientists have now identified a set of SARS-CoV-2-derived molecular mimics that may play a role in initiating autoimmune responses. 3/