2016
DOI: 10.1128/genomea.00869-16
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H9N2 Influenza A Virus Isolated from a Greater White-Fronted Wild Goose ( Anser albifrons ) in Alaska Has a Mutation in the PB2 Gene, Which Is Associated with Pathogenicity in Human Pandemic 2009 H1N1

Abstract: We report here the genomic sequence of an H9N2 influenza A virus [A/greater white-fronted goose/Alaska/81081/2008 (H9N2)]. This virus shares ≥99.8% identity with a previously reported virus. Both strains contain a G590S mutation in the polymerase basic 2 (PB2) gene, which is a pathogenicity marker in the pandemic 2009 H1N1 virus when combined with R591.

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Cited by 4 publications
(2 citation statements)
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“…The same researchers described isolating and characterizing several subtypes of HPAI H5Nx viruses of clade 2.3.4.4 between 2016 and 2017 in Russia, one of which, a HPAI H5N5 virus isolated from gull excreta on Russia’s eastern Kamchatka Peninsula, was demonstrated to be virulent in laboratory mice [ 99 ]. Finally, a H9N2 IAV with mutations associated with infections in humans was isolated in Alaska in 2008 [ 107 ]. Among mammalian hosts in Arctic regions, antibodies against HPAI H7N7 virus were detected in ringed seals in Alaska and the Central Russian Arctic [ 44 , 84 ].…”
Section: Host–pathogen–environmental Ecology Of Iavs In Arctic Regionsmentioning
confidence: 99%
“…The same researchers described isolating and characterizing several subtypes of HPAI H5Nx viruses of clade 2.3.4.4 between 2016 and 2017 in Russia, one of which, a HPAI H5N5 virus isolated from gull excreta on Russia’s eastern Kamchatka Peninsula, was demonstrated to be virulent in laboratory mice [ 99 ]. Finally, a H9N2 IAV with mutations associated with infections in humans was isolated in Alaska in 2008 [ 107 ]. Among mammalian hosts in Arctic regions, antibodies against HPAI H7N7 virus were detected in ringed seals in Alaska and the Central Russian Arctic [ 44 , 84 ].…”
Section: Host–pathogen–environmental Ecology Of Iavs In Arctic Regionsmentioning
confidence: 99%
“…Amino acid substitutions in PB2-M631L and PB2-E712D have been found to strongly upregulate the viral RNA polymerase and therefore disease severity. A recent study reported both PB2-Q591K and G590S were related to enhancing the pathogenicity in the mammalian host [36]. Amino acid substitutions at T271A, V661A and V683T/A684S in PB2 were identified to contribute to the increasing activity and relate to enhancing the polymerase activity in low temperature [37].…”
Section: Polymerase Basic 2 (Pb2) and Mutationsmentioning
confidence: 95%