Abstract
H9N2 avian influenza viruses are present in poultry worldwide. These viruses are considered to have pandemic potential, because recent isolates can recognize human-type receptor and several sporadic human infections have been reported. In this study, we aimed to identify mutations related to mammalian adaptation of H9N2 influenza virus. We found that mouse-adapted viruses had several mutations in hemagglutinin (HA), PB2, PA, and PB1. Among the detected mutations, PB1-K577E was a novel mutation that had not been previously reported to involve mammalian adaptation. A recombinant H9N2 virus bearing only the PB1-K577E mutation showed enhanced pathogenicity in mice, with increased virus titers in nasal turbinates compared to that in mice infected with the wild-type virus. In addition, the PB1-K577E mutation increased virus polymerase activity in human cell culture at a lower temperature. These data suggest that the PB1-K577E mutation is a novel pathogenicity determinant of H9N2 virus in mice and could be a signature for mammalian adaptation.
Highlights
The natural reservoirs of influenza A viruses are aquatic birds; these viruses are occasionally transmitted to fowl or mammals
H9N2 avian poultry andand sporadic infections infections in humans are a public health concern, as the virus has the potential to become a pandemic in humans are a public health concern, as the virus has the potential to become a pandemic virus
For aFor new pandemic to emerge, the virus mustmust obtain certain mutations that that allow it to adapt to humans
Summary
The natural reservoirs of influenza A viruses are aquatic birds; these viruses are occasionally transmitted to fowl or mammals. The H1, H2, H3, H5, H6, H7, H9, and H10 subtypes of influenza A viruses have been shown to infect humans [1,2,3,4,5]. Among these subtypes, only H1, H2, and H3 have become endemic in humans as seasonal flu. In addition to infection with the H9N2 virus itself, some of the H9N2 virus genes were transferred to highly pathogenic H5N1 and H7N9 viruses; and the first human infections with these viruses were reported in Hong Kong in 1997 and China in 2013, respectively [11,12,13]
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