A-Z Index × Submit A-Z Index × Submit A-Z Index Search Dropdown × Submit Facebook Twitter LinkedIn Syndicate Emerging Infectious Disease journal ISSN: 1080-6059 Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.
Highly pathogenic avian influenza H5NX clade 2.3.4.4b viruses continue to circulate globally. Reintroduction of Eurasian lineage viruses into North America and reassortment with endemic low pathogenicity strains have resulted in new genotypes, including D1.2. To assess pathogenicity and cellular tropism, we intranasally inoculated genotype D1.2 virus into pigs. We isolated virus from nasal secretions from most inoculated animals for multiple days. At 5 days postinoculation, PCR and immunohistochemistry detected virus in musculoskeletal, respiratory, digestive, lymphatic, and nervous systems and isolates from meat juice. At 35 days postinoculation, we detected viral antigen and low levels of RNA in the brain of an animal with lesions consistent with a viral etiology and found viral antigen in the ethmoid of 2 animals. Consistent detection in nasal swab specimens, combined with subclinical respiratory infection, systemic distribution, and protracted detection of clade 2.3.4.4b virus in swine, suggest identifying infection in commercial swine without overt respiratory signs could be difficult.
Influenza A viruses (IAVs) remain the most common cause of pandemics ( 1 ). Highly pathogenic avian influenza (HPAI) A virus strains belonging to the goose/Guangdong H5NX lineage (Gs/Gd) have pandemic potential. Continued circulation and reintroductions have resulted in numerous genotypes within H5NX clade 2.3.4.4b viruses because of reassortment with low pathogenicity avian influenza A viruses (LPAIV) ( 2 – 5 ). In addition, the ecology of currently circulating H5NX clade 2.3.4.4b viruses has become increasingly complex, including continued circulation in a broad range of wild birds, frequent spillover into mammals, and mammal-to-mammal transmission in multiple environments ( 5 , 6 ). Across those different infected species, clinical disease and pathology are variable. Mammal-to-mammal or avian-to-mammal transmission has led to a subset of strains that contain known mammalian adaptation markers ( 7 , 8 ).
Swine have historically been considered an intermediary host and mixing vessel for avian influenza viruses that can lead to mammalian adaptation and in which novel viruses with pandemic potential might be generated ( 9 ). Swine can be naturally infected with avian IAVs , human IAVs, and endemic swine-adapted IAVs and can express sialic acid receptors for both mammalian and avian IAVs in their respiratory epithelium ( 10 ). The introduction and subsequent reassortment of avian and human IAVs in the swine population have driven the expansion of swine IAV genetic diversity, resulting in all endemic swine IAV in the United States containing human-origin gene segments ( 11 , 12 ). Whereas host adaptation might require multiple mutations, reassortment of a non–host-adapted IAV and a host-adapted IAV can enable the virus to jump many of those barriers ( 13 , 14 ).
On October 29, 2024, HPAI H5N1 clade 2.3.4.4b genotype D1.2 was confirmed in 1 sow housed in a backyard animal holding in Oregon, USA ( 15 ). We sought to assess the pathogenicity and cellular tropism of an HPAI H5N1 strain that was collected from that Oregon far…