Dataset Information

Complete genome sequence of a mammalian species-infectious and -pathogenic H6N5 avian influenza virus without evidence of adaptation.

ABSTRACT: An H6N5 avian influenza virus (AIV) strain, designated A/aquatic bird/Korea/CN5/2009 (H6N5), was isolated from fecal swabs of aquatic birds in 2009, and surprisingly, it showed infectivity and pathogenicity in mammalian species without evidence of adaptation. In this study, we report the first complete genome sequence containing 3' and 5' noncoding regions (NCRs) of a mammalian species-infectious and pathogenic H6N5 AIV, which will help provide important insights into the molecular basis of pathogenesis, transmission, and evolution of AIV.

SUBMITTER: Park SJ

PROVIDER: S-EPMC3486463 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

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Complete genome sequence of a mammalian species-infectious and -pathogenic H6N5 avian influenza virus without evidence of adaptation.

Park Seong-Jun SJ Park Bong-Kyun BK Song Dae-Sub DS Poo Haryoung H

Journal of virology 20121101 22

An H6N5 avian influenza virus (AIV) strain, designated A/aquatic bird/Korea/CN5/2009 (H6N5), was isolated from fecal swabs of aquatic birds in 2009, and surprisingly, it showed infectivity and pathogenicity in mammalian species without evidence of adaptation. In this study, we report the first complete genome sequence containing 3' and 5' noncoding regions (NCRs) of a mammalian species-infectious and pathogenic H6N5 AIV, which will help provide important insights into the molecular basis of path ...[more]

PMID: 23087119

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Project description:Influenza A viruses (IAVs) are common pathogens of birds that occasionally establish endemic infections in mammals. The processes and mechanisms that result in IAV mammalian adaptation are poorly understood. The viral nonstructural 1 (NS1) protein counteracts the interferon (IFN) response, a central component of the host species barrier. We characterized the NS1 proteins of equine influenza virus (EIV), a mammalian IAV lineage of avian origin. We showed that evolutionarily distinct NS1 proteins counteract the IFN response using different and mutually exclusive mechanisms: while the NS1 proteins of early EIVs block general gene expression by binding to cellular polyadenylation-specific factor 30 (CPSF30), NS1 proteins from more evolved EIVs specifically block the induction of IFN-stimulated genes by interfering with the JAK/STAT pathway. These contrasting anti-IFN strategies are associated with two mutations that appeared sequentially and were rapidly selected for during EIV evolution, highlighting the importance of evolutionary processes in immune evasion mechanisms during IAV adaptation.IMPORTANCE Influenza A viruses (IAVs) infect certain avian reservoir species and occasionally transfer to and cause epidemics of infections in some mammalian hosts. However, the processes by which IAVs gain the ability to efficiently infect and transmit in mammals remain unclear. H3N8 equine influenza virus (EIV) is an avian-origin virus that successfully established a new lineage in horses in the early 1960s and is currently circulating worldwide in the equine population. Here, we analyzed the molecular evolution of the virulence factor nonstructural protein 1 (NS1) and show that NS1 proteins from different time periods after EIV emergence counteract the host innate immune response using contrasting strategies, which are associated with two mutations that appeared sequentially during EIV evolution. The results shown here indicate that the interplay between virus evolution and immune evasion plays a key role in IAV mammalian adaptation.

Project description:UnlabelledHighly pathogenic H5N1 influenza A viruses continue to circulate among avian species and cause sporadic cases of human infection. Therefore, the threat of a pandemic persists. However, the human cases of H5N1 infection have been limited mainly to individuals in close contact with infected poultry. These findings suggest that the H5N1 viruses need to acquire adaptive mutations to gain a replicative advantage in mammalian cells to break through the species barrier. Many amino acid mutations of the polymerase complex have been reported to enhance H5N1 virus growth in mammalian cells; however, the mechanism for H5N1 virus of adaptation to humans remains unclear. Here, we propose that the PA of an H5N1 influenza virus isolated from a human in Vietnam (A/Vietnam/UT36285/2010 [36285]) increased the ability of an avian H5N1 virus (A/chicken/Vietnam/TY31/2005 [Ck/TY31]) to grow in human lung epithelial A549 cells. The five PA amino acid substitutions V44I, V127A, C241Y, A343T, and I573V, which are rare in H5N1 viruses from human and avian sources, enhanced the growth capability of this virus in A549 cells. Moreover, these mutations increased the pathogenicity of the virus in mice, suggesting that they contribute to adaptation to mammalian hosts. Intriguingly, PA-241Y, which 36285 encodes, is conserved in more than 90% of human seasonal H1N1 viruses, suggesting that PA-241Y contributes to virus adaptation to human lung cells and mammalian hosts.ImportanceMany amino acid substitutions in highly pathogenic H5N1 avian influenza viruses have been shown to contribute to adaptation to mammalian hosts. However, no naturally isolated H5N1 virus has caused extensive human-to-human transmission, suggesting that additional, as-yet unidentified amino acid mutations are needed for adaptation to humans. Here, we report that five amino acid substitutions in PA (V44I, V127A, C241Y, A343T, and I573V) contribute to the replicative efficiency of H5N1 viruses in human lung cells and to high virulence in mice. These results are helpful for assessing the pandemic risk of isolates and further our understanding of the mechanism of H5N1 virus adaptation to mammalian hosts.

Dataset Information

Complete genome sequence of a mammalian species-infectious and -pathogenic H6N5 avian influenza virus without evidence of adaptation.

Publications

Complete genome sequence of a mammalian species-infectious and -pathogenic H6N5 avian influenza virus without evidence of adaptation.

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