Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Poultry Farm Workers, Washington, USA, 2024
Abstract
Poultry workers in Washington, USA, were infected with highly pathogenic avian influenza A(H5N1) virus and recovered. The viruses were clade 2.3.4.4b genotype D1.1, closely related to viruses causing poultry outbreaks. Continued surveillance and testing for influenza A(H5) clade 2.3.4.4b viruses remain essential for risk assessment and pandemic preparedness of zoonotic influenza viruses.
The global spread of A/goose/Guangdong/96-lineage highly pathogenic avian influenza (HPAI) virus of the A(H5) subtype has resulted in numerous clades, subclades, and genotypes because of continuous genetic drift and reassortment. HPAI H5N1 clade 2.3.4.4b virus is the most widespread globally; since December 2021, that clade has circulated in wild birds in the United States, affecting millions of poultry, mammalian wildlife, domestic livestock, and companion animals (1,2). In 2024, two distinct genotypes were mainly responsible for ongoing outbreaks in the United States, B3.13 mostly in dairy cattle and D1.1 in poultry, but outbreaks of both genotypes were reported in cattle and poultry (3,4).
Sporadic human infections with clade 2.3.4.4b viruses have also been reported in the United States. During April 1, 2024–June 30, 2025, a total of 70 human cases were reported, including 41 cases after dairy cattle exposure, 24 after exposure to commercial poultry flocks, 2 after exposure to backyard flocks, and 3 with an unknown exposure source (5,6). In response to reported human infections with clade 2.3.4.4b viruses in the United States and other countries, several 2.3.4.4b A(H5) prepandemic candidate vaccine viruses (CVVs) have been made available for pandemic influenza preparedness (7).
In late 2024, the Washington State Public Health Laboratory detected influenza A(H5) virus by real-time reverse transcription PCR among specimens from poultry workers experiencing influenza symptoms. We investigated virus isolates from human cases in Washington to determine virus receptor-binding preference and cross-reactivity with existing CVVs.
