NIH-Funded Researchers Engineer Drug-Resistant Bat-Human Hybrid Influenza Viruses in Missouri: Journal 'Pathogens'
Created using reverse genetics and replicate better in mammalian cells.
A new peer-reviewed study confirms that U.S. National Institutes of Health (NIH)–funded scientists have genetically engineered bat-human hybrid influenza viruses using reverse genetics in Missouri.
These purported viruses are resistant to common antivirals, capable of replicating in mammalian cells, and deliberately mutated for drug resistance, raising fears of an accidental or intentional leak.
Published June 18, 2025 in Pathogens, the study was funded by NIH/NIAID grants including 1R01AI134768 and the Centers of Excellence in Influenza Research and Response (CEIRR), contract number 75N93021C00016.
That NIH contract was awarded to principal investigator Dr. Richard Webby of St. Jude Children’s Research Hospital in Memphis, Tennessee, who also serves as Director of the World Health Organization (WHO) Collaborating Centre for Studies on the Ecology of Influenza in Animals and Birds.
The new study was conducted at the University of Missouri’s Department of Veterinary Pathobiology and Center for Influenza and Emerging Infectious Diseases.
“Wild-type bat H17N10 and H18N11 viruses have been successfully generated using reverse genetics,” the researchers wrote, confirming the use of synthetic reconstruction to resurrect novel pathogens never known to infect humans naturally.
The new pathogen creation comes as the NIH continues funding virus enhancement experiments abroad, including a July 2025 Virology Journal paper in which U.S.-backed researchers in China created lab-made influenza viruses using bird, dog, and human pandemic strains—resulting in chimeras that infected human lung cells more efficiently, triggered heightened inflammation, and carried “considerable zoonotic risk.”
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Chimeric Gain-of-Function Virus Construction
The team reportedly created chimeric viruses combining six internal genes from bat influenza viruses (H17N10 or H18N11) with surface genes (HA and NA) from a human-infecting H1N1 strain (A/Puerto Rico/8/1934), forming hybrids that replicate efficiently in Madin-Darby canine kidney (MDCK) cells.
“Chimeric bat influenza viruses...replicate efficiently and induce CPEs [cytopathic effects—which are structural changes in host cells caused by viral infection] in normal substrates for classical IAVs (influenza A viruses),” the study reads.
This construction makes them infectious in mammalian cells, opening the door to potential zoonotic crossover, according to the mainstream virological paradigm.
Engineered for Antiviral Resistance
Researchers confirmed that the bat influenza M2 proteins contain a mutation (N31) known to confer resistance to amantadine, a widely known antiviral drug.
The team then intentionally mutated the M2 protein at key amino acid sites (N31, H37, W41, and L36) to test how changes affected resistance, replication, and survival.
“Chimeric bat influenza viruses with H17N10 or H18N11 M2 carrying N31 are resistant to amantadine,” they wrote. “Jun7-9 shows inhibition against both amantadine-sensitive and -resistant influenza viruses.”
These experiments fall squarely under gain-of-function research, in which viruses are genetically enhanced to exhibit new traits like immune escape or increased replication in host cells.
Mutation Experiments Reveal Survival-Enhancing Changes
Several mutant viruses were created with substitutions at the histidine-37 and tryptophan-41 positions, which govern the proton ion channel essential to viral infectivity.
“Both H37G and W41A substitutions in M2 significantly affect the survival or replication of chimeric viruses in the H17N10 background,” the authors reported.
The stated goal was to determine how these mutations altered infectivity and drug sensitivity.
The team said they succeeded in rescuing several viable mutant strains, but noted that some mutation combinations proved fatal or nonviable in specific genetic backgrounds.
Reverse-Engineered Bat Flu with Pandemic Potential
According to the paper, the viruses were engineered using reverse genetics, a technique involving synthetic assembly of viral genomes from nucleotide sequences.
“To rescue chimeric and recombinant viruses as well as their single- or double-mutant viruses, eight gene plasmids...were mixed and incubated,” the authors wrote, detailing a process that can be used to custom-build viruses not found in nature.
This research is especially controversial in the wake of concerns that lab-based manipulation of viruses may have played a role in the origin of COVID-19.
Congress, the White House, the Department of Energy, the FBI, and the CIA have acknowledged that a lab-related incident involving gain-of-function research is most likely the origin of the COVID pandemic, raising concerns that ongoing experiments like these could trigger another one.
The fact that the viruses were engineered to infect mammalian cells, evade common antivirals, and survive under drug pressure raises serious biosecurity and biosafety concerns.
Funded by U.S. Taxpayers
Despite the contentious nature of gain-of-function research, this project was funded by multiple U.S. government agencies, including:
NIH/NIAID grant 1R01AI134768
Centers of Excellence in Influenza Research and Response (CEIRR), contract 75N93021C00016
University of Missouri Startup Funds
The study received Institutional Biosafety approval from the University of Missouri under protocol #12100.
These developments come amid growing global concern over government-sponsored pandemic potential research and the lack of transparency around laboratory biosafety oversight.
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Is it safe to ask: Is this a Fauci-ian hangover? Or just good old military-industrial capitalism with home grown innovation in the spirit of Dems and MAGA billionaires? Why? Because somebody needs to hold the pandemic market for fear and death in patriotic paws? As I have commented before: I sat in a lecture hall in 1998 to hear the guru of Ebola promote funding scientists for this very kind of thing. One might wonder if these recent publications are just the slow ‘Open Science’ trailing release of something already done in Colorado or some military base or offshore lab.
These scientists are dangerously insane! Unjabbed Mick (UK).