Catastrophic Gain-of-function via one mutation (lab manipulations giving pathogen more infectivity, lethality) is ongoing for H5N1 avian bird flu virus as they are intent on bringing a fake

non-pandemic AGAIN to force on us, across the board mRNA transfection vaccines (transitioning all vaccines to mRNA); new research shows that ONE (1) single mutation in bovine (cows) H5N1

hemagglutinin can induce specificity to human receptors; ‘single glutamine to leucine mutation at residue 226 of the virus hemagglutinin was sufficient to enact the change from avian to human specificity’; ‘Notably, a single Gln²²⁶Leu mutation can completely switch bovine H5 HA to human-type receptor specificity.’

Be warned, these beasts, these malevolent barbarians can gin up the H5N1 and are seeking to via ongoing work. Why would they be doing this? What is the benefit? If they make something more lethal then that is a crime against humanity. This single mutation if they are able to do it in the lab, could have serious consequences.

What is the point of this article? I am saying and calling for a complete ban of all gain-of-function (GoF) or similar type research, and no funding whatsoever via US taxpayers. All such laboratories must be shuttered. I am calling on the heads of CDC, NIH, FDA, NIAID, HHS etc. to impose a complete ban on January 20th, 2025.

A single mutation in bovine influenza H5N1 hemagglutinin switches specificity to human receptors | Science

‘Abstract

In 2024, several human infections with highly pathogenic clade 2.3.4.4b bovine influenza H5N1 viruses in the United States raised concerns about their capability for bovine-to-human or even human-to-human transmission. In this study, analysis of the hemagglutinin (HA) from the first-reported human-infecting bovine H5N1 virus (A/Texas/37/2024, Texas) revealed avian-type receptor binding preference. Notably, a Gln²²⁶Leu substitution switched Texas HA binding specificity to human-type receptors, which was enhanced when combined with an Asn²²⁴Lys mutation. Crystal structures of the Texas HA with avian receptor analog LSTa and its Gln²²⁶Leu mutant with human receptor analog LSTc elucidated the structural basis for this preferential receptor recognition. These findings highlight the need for continuous surveillance of emerging mutations in avian and bovine clade 2.3.4.4b H5N1 viruses.’