Since its emergence in 1968, H3N2 has undergone a considerable number of mutations. It is, in a way the "Omicron" of HxNx viruses with several types :
- H3N2 HUMAN, which was the main strain this winter 2022/23 with in US (CDC) :
2) H3N2 SWINE, which evolved from H2N2 by antigenic shift, and caused the Hong Kong Flu pandemic of 1968 and 1969 that killed between one and four million people globally.
4) H3N2 CANINE, which was identified in Asia during the 2000s with a mutation that adapted from its avian influenza origins and was recently detected in US.
An interesting and simple 😂😂😂 study sent by my friend David Joffe :
"Regulation of N-degron recognin-mediated autophagy by the SARS-CoV-2 PLpro ubiquitin deconjugase"
2) The SARS-CoV-2 virus has an ENZYME called PLpro that can remove 'tags' (called ubiquitin) from host proteins, preventing them from being broken down. The study found that PLpro INTERACTS with enzymes that MARK certain PROTEINS for DESTRUCTION.
3) By keeping these tagged proteins from being broken down, PLpro can change how the cell recycles and gets rid of proteins. This affects a process called AUTOPHAGY, which the virus uses to modify the cell's internal structures and HIDE from the IMMUNE SYSTEM.
SARS-CoV-2 variants are not simply competing with each other, but are in fact WORKING TOGETHER in a COOPERATIVE MANNER !!! 🤔 pmc.ncbi.nlm.nih.gov/articles/PMC10…
2) This study looked at how different versions of the COVID-19 virus, called variants, have evolved over time. The researchers found that these variants are not just competing with each other, but are actually working together.
3) As new variants emerge, they take in and use the genetic changes (mutations) from previous variants, rather than completely replacing them. This suggests the variants are building on each other's changes, not just trying to beat each other.
WHAT IF TOMORROW, HUMANS were the ONES INFECTING other MAMMALS with H5N1?
The study found that the H5N1 virus isolated from a human dairy worker in Texas (rHPHTX) had mutations that enhanced its replication and pathogenicity (100% mortality) in mammals ! tandfonline.com/doi/full/10.10…
2) The study describes the rescue and characterization of recombinant influenza A(H5N1) viruses isolated from infected cattle and a human dairy worker in Texas. The human-origin virus (rHPhTX) had several unique amino acid substitutions compared to ...
3) ...the cattle-origin virus (rHPbTX), particularly in the polymerase and nonstructural proteins.
In vitro, rHPhTX replicated more efficiently than rHPbTX in mammalian and avian cell lines, despite similar antiviral susceptibility.
Harnessing the Power of Human B Cells: A Rapid Antibody Engineering Platform to Arm Against Emerging H5N1 Threats biorxiv.org/content/10.110…
2) The CODE-HB platform offers a powerful approach to rapidly evolve improved antibodies targeting emerging infectious threats like H5N1 influenza. By harnessing the natural somatic hypermutation mechanisms of human B cells, the researchers demonstrated the ability to ...
3) ...evolve variants of the CR9114 antibody with enhanced binding to the H5 hemagglutinin protein from H5N1 strains.
H5N1 poses a major pandemic risk as it can spread from birds to humans.
UNCOVERING the STRUCTURAL SECRETS of the key SARS-CoV-2 E PROTEIN Ion Channel:
How the T9I Mutation in Omicron Variants Modulates Viral Pathogenicity ?
Again, this remarkable T9I mutation that we've been discussing for the past 2 years in a new study: pubs.acs.org/doi/10.1021/ja…
2) The SARS-CoV-2 E protein forms an ion channel that contributes to the virus's ability to cause disease (pathogenicity). The E protein's transmembrane domain (ETM) contains a network of polar residues that are crucial for its ion conduction function.
3) A key mutation, T9I, is found in the Omicron variants of SARS-CoV-2. This mutation changes a polar threonine residue to a hydrophobic isoleucine at the entrance of the ion channel.