This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: How do we know when an animal virus might pose a risk to humans? Canada confirmed a human case of H5N1 avian influenza (often called "bird flu") in 2024, the first known to have been acquired in Canada.
The patient, a 13-year-old from British Columbia, suffered severe symptoms, including respiratory failure, but recovered with intensive care in a hospital. Understanding how pathogens can switch from animals to humans—as in this case of bird flu—can help researchers and public health agencies prepare for future outbreaks. In a recent study, our lab examined viral mutations in this case and uncovered an unexpected result: The effects of these mutations were inconsistent with the usual warning signs we expect to see in a virus adapted to infect humans.
Public health agencies and collaborating groups use complementary approaches to monitor infectious disease outbreaks and risk. Human outbreak data come from many places, including care settings and associated surveillance labs, volunteers reporting disease status, and wastewater monitoring. Routine virological tests in public health labs include sequencing viral genes, testing for antiviral resistance and assessing immunity against strains of interest.
Through wildlife and agricultural monitoring, Canadian agencies have tracked the arrival of the currently dominant H5N1 lineage of avian influenza, to which the B.C. case belongs. Sequencing of the virus from the patient found three mutations of interest. One is already a well-studied sign of adaptation from birds to mammals.
The other two mutations caught our attention because they are less understood. Both were in hemagglutinin, the viral surface protein that binds to cells and initiates infection by fusing the virus and cell membranes. These mutations, E190D and Q226H (representing 28% and 35%, respectively, of hemagglutinin genetic material sequenced), were in the part of hemagglutinin known to interact with receptors on host cells.
Bird and human cells tend to display different types of receptors, which is why scientists use receptor binding as a common test for species adaptation. These hemagglutinin mutations had not previously been observed to switch binding to human-type receptors in H5N1 influenza. Our lab investigated how these two mutations affected which types of receptors the viruses bind to more readily.
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