The genetic sequence of the H5N1 bird flu virus that infected a teenager in British Columbia shows that the virus had undergone mutational changes that would make it easier for that version of H5N1 to infect people, scientists who have studied the data say. 

There’s currently no evidence the teenager, who remains in critical condition in hospital, infected anyone else. If that’s the case, it is likely this mutated version of the virus would die out when the teen’s illness resolves. The source of the teen’s infection has not been determined, so it’s impossible to know for sure if the mutations were in the virus that infected him or her. But scientists think it is more likely that the mutations developed during the course of his or her infection. Still, the fact that the mutations occurred at all is a reminder that H5N1 is a dangerous virus for people, one that could potentially trigger a pandemic if it acquired the capacity to easily infect people, flu virologists say.

“By no means is this Day 1 of a pandemic. There’s no indication … of human-to-human spread, which is all good. But this is exactly the scenario that we fear,” Scott Hensley, a professor of microbiology at the University of Pennsylvania’s Perelman School of Medicine, told STAT in an interview.

Hensley sparked some concern on social media platforms over the weekend when he remarked on the fact that the genetic sequence of the virus showed key mutational changes in the hemagglutinin, a protein on the virus’ surface that attaches to cells the virus is trying to invade. The sequence data were posted to open-access databases by the Public Health Agency of Canada. 

“This is bad news,” Hensley said in a Bluesky post on Saturday. “We need to closely monitor this situation and increase our surveillance efforts.”

H5N1’s hemagglutinin preferentially binds to cells with receptors known as alpha 2-3, which are abundant in wild birds and domestic poultry, but are also found in the conjunctiva, the tissue surrounding human eyes. The receptors that predominate in human upper airways are known as alpha 2-6, the type to which the human influenza A viruses H1N1 or H3N2 attach. It’s thought that to become a virus capable of spreading easily among people, H5N1 would need to acquire the ability to attach to this latter type of receptor.

Two mutations spotted in the Canadian teen’s virus are known to help flu viruses make this attachment switch. “Both these sites play an important role in … binding specificity,” Jesse Bloom, an evolutionary virologist at the Fred Hutchinson Cancer Center in Seattle, said in a series of posts responding to Hensley. 

Hensley agreed. “Ten out of 10 flu virologists will tell you that these substitutions are important for effective receptor specificity. There’s no question about that.”

The British Columbia case is garnering substantial attention for two reasons. Firstly, how the teenager became infected remains a mystery. Secondly, while H5N1 cases have historically been seen to cause severe disease — and death — in a substantial number of cases, the versions of the virus currently circulating in North America have triggered only mild infections except for in this case.