Possibility of Bird Flu Recurrence

April 20, 2026

A new reassortant highly pathogenic genotype of the avian influenza (HPAI) A(H5N1), commonly known as bird flu, has rapidly spread across the US and Canada, underlining the need for pandemic preparedness.

Clade 2.3.4.4b H5N1 virus, which emerged in late 2021, has affected more than 485 bird species and 48 mammal species worldwide. Now, a new study published in Nature Communications highlights that the new reassortant of genotype D1.1 nearly replaced clade 2.3.4.4b in North America by late 2024.

This genotype was found during the fall migration season of 2024, in September, and was mapped using active and passive methods of avian influenza surveillance across the United States and Canada.

Active surveillance involves samples from apparently healthy birds through live capture or hunter harvest, while passive surveillance includes sick and dead birds.

“These reassortant viruses have caused widespread mortality among wild birds and mammals, with nearly 14,500 wild bird and 650 mammal detections in the US alone,” the study said.It said that Canada recorded HPAI in animals across 12 taxonomic orders and 80 wild bird species within the first year of introduction, with the true scale of impacts likely to be underestimated.

“Since February 2022, HPAI outbreaks have also severely impacted the poultry industry, affecting more than 2,000 US flocks and 186 million birds, and more than 14.5 million birds across 534 flocks in all Canadian provinces,” the authors of the paper said.

They added that there have been 17 reported human A(H5N1) infections caused by genotype D1.1 viruses, of which four were severe and two fatal.

The emergence of the D1.1 viruses aligned with the autumn migration of birds from North American waterfowl towards the south, assisting their dissemination. But the emergence and spread of the virus across North America, and whether the mammalian-adaptive mutations in the human infections originated from wild bird viruses or arose de novo among humans, remain unclear to scientists.

Researchers found that the viruses in these human cases contained mammalian-adaptive markers (such as HA E190D and Q226H substitutions) that were entirely absent from the D1.1 sequences found in wild birds. Because these markers were not found in the bird population, scientists conclude that these mutations likely arose de novo (anew) within the human hosts during the course of the infection, the study said.