PB2 substitutions V598T/I increase the virulence of H7N9 influenza A virus in mammals.PB2 is one of the subunits of the influenza A virus (IAV) polymerase complex.  By bioinformatics analysis we identified PB2 substitutions at positions 389 and 598 among IAV isolates from humans, which might associate with viral pathogenicity.  To evaluate the biological significance of these substitutions, PB2-K389R and -V598T/I mutant viruses of avian H7N9 IAVs were generated by reverse genetics.  Notably, the PB2-V598T/I substitutions substantially increased virus replication and virulence in mice.  Together, we demonstrated that the substitutions PB2-V598T/I contributed to higher IAV replication and virulence in mammals, which added to the knowledge of IAV virulence determinants and benefited the surveillance of IAVs.
PB2
PB2 substitutions V598T/I increase the virulence of H7N9 influenza A virus in mammals.PB2 is one of the subunits of the influenza A virus (IAV) polymerase complex.  By bioinformatics analysis we identified PB2 substitutions at positions 389 and 598 among IAV isolates from humans, which might associate with viral pathogenicity.  To evaluate the biological significance of these substitutions, PB2-K389R and -V598T/I mutant viruses of avian H7N9 IAVs were generated by reverse genetics.  Notably, the PB2-V598T/I substitutions substantially increased virus replication and virulence in mice.  Together, we demonstrated that the substitutions PB2-V598T/I contributed to higher IAV replication and virulence in mammals, which added to the knowledge of IAV virulence determinants and benefited the surveillance of IAVs.
PB2
PB2 substitutions V598T/I increase the virulence of H7N9 influenza A virus in mammals.PB2 is one of the subunits of the influenza A virus (IAV) polymerase complex.  By bioinformatics analysis we identified PB2 substitutions at positions 389 and 598 among IAV isolates from humans, which might associate with viral pathogenicity.  To evaluate the biological significance of these substitutions, PB2-K389R and -V598T/I mutant viruses of avian H7N9 IAVs were generated by reverse genetics.  Notably, the PB2-V598T/I substitutions substantially increased virus replication and virulence in mice.  Together, we demonstrated that the substitutions PB2-V598T/I contributed to higher IAV replication and virulence in mammals, which added to the knowledge of IAV virulence determinants and benefited the surveillance of IAVs.
PB2
PB2 substitutions V598T/I increase the virulence of H7N9 influenza A virus in mammals.PB2 is one of the subunits of the influenza A virus (IAV) polymerase complex.  By bioinformatics analysis we identified PB2 substitutions at positions 389 and 598 among IAV isolates from humans, which might associate with viral pathogenicity.  To evaluate the biological significance of these substitutions, PB2-K389R and -V598T/I mutant viruses of avian H7N9 IAVs were generated by reverse genetics.  Notably, the PB2-V598T/I substitutions substantially increased virus replication and virulence in mice.  Together, we demonstrated that the substitutions PB2-V598T/I contributed to higher IAV replication and virulence in mammals, which added to the knowledge of IAV virulence determinants and benefited the surveillance of IAVs.
PB2
PB2 substitutions V598T/I increase the virulence of H7N9 influenza A virus in mammals.PB2 is one of the subunits of the influenza A virus (IAV) polymerase complex.  By bioinformatics analysis we identified PB2 substitutions at positions 389 and 598 among IAV isolates from humans, which might associate with viral pathogenicity.  To evaluate the biological significance of these substitutions, PB2-K389R and -V598T/I mutant viruses of avian H7N9 IAVs were generated by reverse genetics.  Notably, the PB2-V598T/I substitutions substantially increased virus replication and virulence in mice.  Together, we demonstrated that the substitutions PB2-V598T/I contributed to higher IAV replication and virulence in mammals, which added to the knowledge of IAV virulence determinants and benefited the surveillance of IAVs.
PB2