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2024-4-28 12:44:07


Gu G, Liu C, Lee SH, Chun Choi LS, Wilson MT, Pfei. Detection of a reassortant swine H1N2 influenza A virus from pigs in Hong Kong. Virol Sin. 2024 Feb 1:S1995-820X(24)00009-9
submited by kickingbird at Feb, 4, 2024 14:58 PM from Virol Sin. 2024 Feb 1:S1995-820X(24)00009-9

Influenza A viruses (IAVs) are responsible for significant respiratory illnesses in humans and a broad range of animal species. Repeated outbreaks and the rapid spread of genetically and antigenically distinct IAVs represent a considerable challenge for swine production. Pigs are susceptible to avian and human IAV infections and are considered “mixing vessels” where human, avian, and swine IAVs can recombine and generate novel reassortant influenza viruses with pandemic potential (Vincent et al., 2014). Presently, three major swine IAV subtypes, H1N1, H1N2, and H3N2, are circulating globally (Komadina et al., 2014). The classical swine (CS) A(H1N1) virus, which originated from the 1918 human H1N1 virus, is prevalent in the Americas and Asia (Webster et al., 1992). In the late 1970s, the Eurasian “avian-like” (EA) A(H1N1) subtype emerged as a result of the adaptation of the avian H1N1 IAVs in pigs, which soon became predominant in Europe (Pensaert et al., 1981). Similarly, human-like swine A(H3N2) influenza viruses emerged in Taiwan region after the human A(H3N2) pandemic in 1968 (Komadina et al., 2014). Later in the 1980s, the swine influenza A(H1N2) virus was generated through the reassortment of classical swine A(H1N1) and human A(H3N2) viruses and isolated from pigs in France and Japan (Komadina et al., 2014). In 1999, triple-reassortant influenza (TRIG) A(H1N2) viruses containing NA and PB1 genes of the human A(H3N2) virus, HA, M, NP, and NS genes of CS A(H1N1) virus, and PB2 and PA genes of avian influenza viruses were reported from pigs in North America (Karasin et al., 2002). In 2009, the pandemic H1N1/2009 (H1N1pdm09) viruses, containing M and NA gene segments derived from the EA A(H1N1) viruses and the remaining genes from TRIG A(H1N2) viruses, emerged and rapidly spread in humans and swine worldwide. Consequently, the co-circulation of the H1N1pdm09 viruses with pre-existing influenza H1N1, H3N2, and H1N2 viruses in pigs contributed to generating novel reassortants, complicating the epidemiology of swine influenza (Komadina et al., 2014).

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