Bird flu virus is one mutation away from binding more efficiently to human cells

Scientists have identified that H5N1, the highly pathogenic avian influenza virus currently spreading among U.S. dairy cows, requires only a single mutation to latch onto human cells in the upper airway. The study, published today in Science, reveals a simple genetic pathway for the virus to potentially enhance its ability to transmit between humans—raising concerns about its pandemic potential if such a mutation occurs in nature.

Avian influenza viruses are equipped with surface proteins that enable them to bind to bird cell receptors, facilitating viral entry. Bird cell receptors differ only subtly from those in humans, explains James Paulson, a biochemist at Scripps Research and co-author of the study. “For an H5N1 virus to spark a new pandemic, it must shift its receptor preference from avian to human. The surprising finding is that this shift only requires one genetic change.”

The specific clade of H5N1 driving the current outbreak was first detected in North America in 2021 and has since infected a variety of species, including wild birds, foxes, bears, marine mammals, and recently, dairy cows. Since outbreaks began in U.S. dairy herds this spring, human cases have primarily involved farmworkers exposed to infected poultry or cows. Most infections have been mild, and there is no evidence of human-to-human transmission so far. A major barrier to such transmission is the virus’s limited ability to bind to human cell receptors.

“It’s speculative but concerning,” says Jenna Guthmiller, an immunologist at the University of Colorado Anschutz Medical Campus who was not involved in the study. “If the virus becomes better at binding to human receptors, it increases the likelihood of human-to-human transmission.”

The researchers focused on hemagglutinin, a surface protein on H5N1 that enables the virus to bind to host cell receptors and initiate infection. Using genetic sequences from the first human case in Texas—linked to exposure to an infected cow—the scientists engineered various mutations into hemagglutinin. Without using live virus, they found that a single mutation substituting the 226th amino acid in hemagglutinin allowed the virus to shift its binding preference from bird receptors to human receptors in the upper respiratory tract.

These findings highlight how minimal genetic changes could increase the threat of H5N1 to humans, underscoring the importance of ongoing surveillance and preventative measures.

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