1. Pigs are highly susceptible to but do not transmit mink-derived highly pathogenic avian influenza virus H5N1 clade 2.3.4.4b.
- Author
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Kwon T, Trujillo JD, Carossino M, Lyoo EL, McDowell CD, Cool K, Matias-Ferreyra FS, Jeevan T, Morozov I, Gaudreault NN, Balasuriya UBR, Webby RJ, Osterrieder N, and Richt JA
- Subjects
- Animals, Swine, Spain, Viral Proteins genetics, Viral Proteins metabolism, Virus Shedding, Mink virology, Orthomyxoviridae Infections virology, Orthomyxoviridae Infections transmission, Orthomyxoviridae Infections veterinary, Influenza A Virus, H5N1 Subtype pathogenicity, Influenza A Virus, H5N1 Subtype genetics, Influenza A Virus, H5N1 Subtype physiology, Influenza A Virus, H5N1 Subtype isolation & purification, Swine Diseases virology, Swine Diseases transmission
- Abstract
ABSTRACT Rapid evolution of highly pathogenic avian influenza viruses (HPAIVs) is driven by antigenic drift but also by reassortment, which might result in robust replication in and transmission to mammals. Recently, spillover of clade 2.3.4.4b HPAIV to mammals including humans, and their transmission between mammalian species has been reported. This study aimed to evaluate the pathogenicity and transmissibility of a mink-derived clade 2.3.4.4b H5N1 HPAIV isolate from Spain in pigs. Experimental infection caused interstitial pneumonia with necrotizing bronchiolitis with high titers of virus present in the lower respiratory tract and 100% seroconversion. Infected pigs shed limited amount of virus, and importantly, there was no transmission to contact pigs. Notably, critical mammalian-like adaptations such as PB2-E627 K and HA-Q222L emerged at low frequencies in principal-infected pigs. It is concluded that pigs are highly susceptible to infection with the mink-derived clade 2.3.4.4b H5N1 HPAIV and provide a favorable environment for HPAIV to acquire mammalian-like adaptations.
- Published
- 2024
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