Since the bird flu tale second grew up post-COVID, we’ve been waiting for the other foot to fall for a couple of years.
Given that the medical protection state is actually funding gain-of-function study on viruses in clandestine labs all over the world, completely defensive from oversight, mammal-to-mammal gain-of-function, or the newly discovered ability to transmit between mammals, has always seemed expected.
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Robert Redfield, a former CDC Director, predicted bioengineered bird flu, which infects and spreads among people, was “drop in months.”
Previous CDC Director Says , Bird Flu May Be Lab-Produced in Humans in Times.
Via Nature, March 6, 2025 (emphasis added ):
In Chile in December 2022, highly pathogenic H5N1 avian influenza viruses ( HPAIV ) from lineage 2.3.4.4b emerged, causing mass mortalities in wild birds, poultry, and marine mammals, as well as one human case. We sequenced 177 H5N1 virus genomes from poultry, marine mammals, a human, and wild birds, which span 3800 km of Chilean coastline, and found HPAIV in 7, 33 % ( 714/9745 ) of cases between December 2022 and April 2023. Similar to Peru’s H5N1 outbreak, which had a north-to-south spread along the Pacific coast, Chilean pathogens were closely related. Despite being sampled 5 days and hundreds of kilometers off, one human disease and nine marine animal infections in Chile shared the uncommon PB2 D701N mammalian-adaptation gene and clustered evolutionarily. These viruses shared additional genetic signatures, including a second mammalian PB2 adaptation ( Q591K, n = 6), synonymous mutations, and minor variations. Months later, sealions in the Atlantic coast were found to have a number of variants, suggesting that the pinniped epidemics on the west and east coastlines of South America are physically related. These results demonstrate that HPAIV was successfully transmitted by sea mammals over thousands of kilometers of Chile’s Pacific peninsula, which later spread through the Atlantic coast.
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The  , particular systems by which the new bird flu strain probably becomes more spreadable in and among humans include bound to a protein called importin- and neutralizing/evading the immune response, depending on how much property we can put in the protein sequencing.
Continuing:
Due to the possibility of zoonotic transmission, the HPAIV H5N1 virus translation to mammals is a major epidemic issue. In mammal hosts, including humans, the D701N gene has been shown to increase viral replication and infectivity. By bound to human importin-, this gene may increase the viral ribonucleoprotein (vRNP ) nuclear trade. In contrast to the well-known 627 K mammal adaptation mutation, which is responsible for the virus’s increased propagation and transmission in mammals, the Q591K gene has also been attributed to a compensatory mutation. It is thought that an interaction with an antagonistic host protein is halted by the favorable charge associated with both the PB2-627K and 591 K. Note that the 627 K has not been found so far in the South American infections, in striking contrast to previous outbreaks in Southeast Asia, Europe, and North America.
Trump to stop gain-of-function studies from being halted through an executive order, according to a report.
These reported minor changes to a popular genome, whether natural or artificial, could mean the difference between life as it is continuing and a whole new round of world anxiety, lockdowns, novel mRNA vaccines, and other Public HealthTM impositions. We should guess on the latter until the evidence is proven otherwise.  ,
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