by Jon Fleetwood, Jon Fleetwood:
HHS-backed research produced chimeric influenza viruses carrying SARS-CoV-2’s ACE2-binding interface—introducing a higher-affinity human receptor-binding mechanism into an influenza pathogen.
HHS-funded researchers are claiming to have engineered influenza-based chimeric “Frankenstein” viruses that combine influenza’s hemagglutinin (HA) with the SARS-CoV-2 receptor-binding domain (RBD)—a high-affinity human ACE2-binding interface.
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Introducing a fundamentally different and stronger human cell–binding mechanism into an influenza viral system is a modification that fits longstanding U.S. gain-of-function definitions involving altered receptor usage and host range.
A December 2025 bioRxiv preprint confirms the work, supported in part by the National Institutes of Health (NIH)—an agency within the U.S. Department of Health and Human Services (HHS)—was funded under grant P01-AI165075:
“This work was funded by… National Institutes of Health… P01-AI165075”
and involved replacing influenza’s native HA gene with the SARS-CoV-2 RBD while producing virus particles coated with HA in the laboratory, resulting in viral constructs that physically contain both influenza’s entry protein and the SARS-CoV-2 optimized human cell–binding interface.
The study was conducted by Jonathan Munro, Diana Melnyk, Madeeha Afzal, Lisa Schimanski, Alexander A. Cohen, Jennifer R. Keeffe, Pamela J. Bjorkman, William S. James, Alain R. Townsend, and Tiong Kit Tan, with affiliations including the University of Oxford’s Weatherall Institute of Molecular Medicine and Sir William Dunn School of Pathology (here), the Chinese Academy of Medical Sciences–Oxford Institute (here), and the California Institute of Technology (here).
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