Reckless H5N1 Bird Flu Gain-of-Function Experiments Must Be Shut Down

by Nicolas Hulscher, MPH

Please enjoy my interview on Reality Check Radio with Paul Brennan, where we discuss bird flu and the dark history of H5N1 gain of function research, including our recently published study, Proximal Origin of Epidemic Highly Pathogenic Avian Influenza H5N1 Clade 2.3.4.4b and Spread by Migratory Waterfowl, and the recent H7N6 bird flu outbreak on a New Zealand farm.

Here are the key points about bird flu:

1. Practice of culling (mass destruction of entire healthy flocks) when a PCR test is found positive to “eradicate” the virus is futile and may work to constrain the food supply. The current strain H5N1 clade 2.3.4.4.b is not thus far causing necropsy or radiographic confirmed fatal pneumonia in birds or mammals.

2. H5N1 host range expansion into migratory birds and mammals likely occurred as a result of gain-of-function serial passage research and a lab leak.

3. Increased transmissibility of H5N1 has a tradeoff of decreased virulence. Using legacy human mortality rates from cases in Southeast Asia is not appropriate. The US has never had a fatal human case of bird flu.

4. Fear-mongering promulgated by the Bio-Pharmaceutical Complex is designed to promote mass vaccination of animals and humans with lucrative pre-purchased contracts to the vaccine manufacturers and their NGO backers. Mass vaccination into a highly prevalent pandemic is a mistake since it promotes resistant strains of the virus in the vaccinated.

5. If human-to-human spread occurs in the future as expected by many, it will be the product of gain-of-function research that has gone on for years with the goal of creating harm to human populations.

Reckless H5N1 gain-of-function research continues with minimal oversight. Recently, an NIH and Bill Gates-funded California BSL-3 biolab mutated H5N1 bird flu with gain-of-function experiments, publishing the blueprints needed for bioterrorists in the journal Science:

To assess the potential for the recent 2.3.4.4b viruses to acquire human-type receptor specificity, we introduced mutations into the receptor binding site (RBS) of the Texas HA protein and assessed receptor binding using surface plasmon resonance (SPR), enzyme-linked immunosorbent assay (ELISA), and glycan array analyses. Furthermore, we determined crystal structures for Texas H5 HA and its Gln226Leu mutant with avian and human receptor analogs to provide insights into the molecular basis of H5 HA receptor preference.

Because each mutation is independent and the probability of achieving additional mutations decreases exponentially, our observation that a single mutation is sufficient to switch receptor specificity in the Texas HA dramatically increases the likelihood of achieving this phenotype required for human transmission.

There must be an immediate and complete global moratorium on gain-of-function research, along with comprehensive investigations into the growing number of U.S. and international biolabs—including their funders—that may be conducting bioweapon research, to prevent another man-made pandemic.

Nicolas Hulscher, MPH

Epidemiologist and Foundation Administrator, McCullough Foundation

www.mcculloughfnd.org

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