We’ve been waiting for the other shoe to drop for a couple of years at this point since the bird flu narrative first ramped up post-COVID.
Mammal-to-mammal gain-of function — the newfound ability to transmit between mammals — has always seemed inevitable, given that the biomedical security state is literally funding gain-of-function research on viruses in clandestine labs all over the world, fully immune from oversight.
It was nearly a year ago that former CDC Director Robert Redfield predicated bioengineered bird flu that infects and transmits among humans could drop “in months.”
Related: Bird Flu Engineered to Infect Humans Could Be Lab-Produced ‘in Months,’ Former CDC Director Says
Via Nature, March 6, 2025 (emphasis added):
Highly pathogenic H5N1 avian influenza viruses (HPAIV) belonging to lineage 2.3.4.4b emerged in Chile in December 2022, leading to mass mortality events in wild birds, poultry, and marine mammals and one human case. We detected HPAIV in 7,33% (714/9745) of cases between December 2022–April 2023 and sequenced 177 H5N1 virus genomes from poultry, marine mammals, a human, and wild birds spanning >3800 km of Chilean coastline. Chilean viruses were closely related to Peru’s H5N1 outbreak, consistent with north-to-south spread down the Pacific coastline. One human virus and nine marine mammal viruses in Chile had the rare PB2 D701N mammalian-adaptation mutation and clustered phylogenetically despite being sampled 5 weeks and hundreds of kilometers apart. These viruses shared additional genetic signatures, including another mammalian PB2 adaptation (Q591K, n = 6), synonymous mutations, and minor variants. Several mutations were detected months later in sealions in the Atlantic coast, indicating that the pinniped outbreaks on the west and east coasts of South America are genetically linked. These data support sustained mammal-to-mammal transmission of HPAIV in marine mammals over thousands of kilometers of Chile’s Pacific coastline, which subsequently continued through the Atlantic coastline.
Depending on how much stock we can put in the gene sequencing, the specific mechanisms by which the new bird flu strain potentially becomes more infectious in and among humans includes binding to a protein called importin-α and neutralizing/evading the immune response.
Continuing:
Adaptation of the HPAIV H5N1 viruses to mammals is a significant pandemic concern due to its potential for zoonotic transmission. The D701N mutation has been shown to enhance viral replication and pathogenicity in mammalian hosts, including humans. This mutation can enhance the nuclear import of the viral ribonucleoprotein (vRNP) by binding to human importin-α. The Q591K mutation has also been implicated in increased replication and transmission of the virus in mammals, and it has been identified as a compensatory mutation in the absence of the well-recognized 627 K mammalian adaptation mutation. The positive charge associated with both the PB2-627K or 591 K is thought to disrupt an interaction with an inhibitory host protein. Of note, in stark contrast to previous outbreaks in Southeast Asia, Europe, and North America, the 627 K has not been detected so far in the South American viruses.
Related: Trump to Halt Gain-of-Function Viral Research Via Executive Order, Per Report
Whether natural or souped-up— and we should bet on the latter until proven otherwise — these reported tiny changes to a viral genome could mean the difference between life as normal, such as it is, continuing and a whole new round of global panic, lockdowns, novel mRNA vaccines, and other Public Health™ impositions.
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