H5N1 is currently a ZOONOTIC OUTBREAK, NOT A PANDEMIC !!!
For over two years, we have been raising concerns about the transmission of this virus from birds to mammals, and subsequently to humans.
At this time, H5N1 remains a zoonotic outbreak, which is characterized by ...
2) ...a sudden rise in disease cases from animals to humans within a specific area or population.
Even if we are at stage 3 in the virus's progression, (as I indicated in my last thread 👇), for H5N1 to be classified as a pandemic ...
2) The study examined brain tissue from COVID-19 patients and found:
- Low levels of the virus in the brain, suggesting the neurological effects are not mainly due to direct viral infection.
- Widespread problems with energy production and communication between brain cells ...
3) ...especially in certain neuron types. These changes overlap with what's seen in neurodegenerative diseases like Parkinson's and Alzheimer's.
- Increased inflammation and oxidative stress in non-neuronal brain cells, which could contribute to neurodegeneration.
2) Brief summary :
The evolution of SARS-CoV-2 variants has led to structural changes in Spike protein, key for immune response. High-resolution cryo-EM analysis of variants like Alpha and Delta showed no virion morphology changes, but amino acid shifts affected spike dynamics.
3) The illustrations from this study are undeniably the most impressive I've encountered this year.
Figure EV1. SARS-CoV-2 S mutations and the phylogenetic tree.
Pro-inflammatory CYTOKINE IL-1β can potently INHIBIT SARS-CoV-2-induced CELL-CELL FUSION and viral transmission, revealing a critical ANTIVIRAL FUNCTION of INNATE IMMUNE factors. biorxiv.org/content/10.110…
2) The study found that immune cells release factors that can prevent the fusion of SARS-CoV-2-infected cells with neighboring cells, a process called syncytia formation. This is important because syncytia can help the virus spread more easily.
3) One key factor identified was interleukin-1β (IL-1β). IL-1β was able to block syncytia formation by activating a signaling pathway that leads to the formation of actin bundles at the junctions between infected and uninfected cells.
2) This study used computer simulations to understand how the H5N1 influenza virus is changing over time. The researchers looked at how 1,804 different versions of the virus' key protein (hemagglutinin) interact with 11 antibodies that can neutralize the virus.
3) The results show a concerning trend - the virus is becoming less vulnerable to these antibodies as it evolves. This suggests the virus is finding ways to escape our medical defenses.
The researchers also traced the spread of H5N1 between birds and mammals across the world.
How SEVERE a person's COVID-19 ILLNESS will be, based on the GENETICS of the SARS-CoV-2 VIRUS ?
The model was trained on a large dataset of over 158,000 virus genome sequences and patient details collected over 4 years ! nature.com/articles/s4159…
2) The key findings are:
- The model identified over 40 specific mutations in the SARS-CoV-2 genome that increase the risk of severe COVID-19 illness.
- Certain mutations in the virus's spike protein, nucleocapsid protein, and other genes were linked to more severe disease.
3) - Deletions in some viral genes were also found to increase severity.
By analyzing the virus genetics, the model was able to provide insights into how specific genetic changes in SARS-CoV-2 impact the severity of COVID-19.