Risk of Environmental Exposure to H7N9 Influenza Virus via Airborne and Surface Routes in a Live Poultry Market in Hebei, China.
PMID: 34164347
2021
Frontiers in cellular and infection microbiology
Discussion: Some studies have shown that an H9N2 strain with the E627K and Q591K mutations in PB2 was more pathogenic in mice than the unmutated H9N2 strain.
Replication of a Dog-Origin H6N1 Influenza Virus in Cell Culture and Mice.
Introduction: Mutations on these RNP component proteins could change the viral polymerase activity and virulence, such as PA P190S and PA Q400P in H7N3, PA T97I in H6N1, PB1 T296R in H1N1, PB2 E627K in H7N9 and PB2 Q591K in H9N2.
Dynamic PB2-E627K substitution of influenza H7N9 virus indicates the in vivo genetic tuning and rapid host adaptation.
Discussion: In addition to E627K and D701N, previous studies also identified a series of other mammalian adaptation substitutions (e.g., Q591K on the basic surface PB2 of influenza virus) that may have compensatory functions in the activity of polymerase complexes of influenza viruses.
PA from a Recent H9N2 (G1-Like) Avian Influenza a Virus (AIV) Strain Carrying Lysine 367 Confers Altered Replication Efficiency and Pathogenicity to Contemporaneous H5N1 in Mammalian Systems.
Result: Unlike Q591K, the impact of the R367K substitution in the PA on the replication efficiency, polymerase activity and virulence of H5N1 strains has not been characterized yet.
Host ANP32A mediates the assembly of the influenza virus replicase.
Introduction: PB2 V614 is equivalent to K591 in the swine origin 2009 H1N1 pandemic influenza A virus, which retained E627 in its avian PB2 but used a Q591K adaptation to increase polymerase activity (Extended Data.
PA Mutations Inherited during Viral Evolution Act Cooperatively To Increase Replication of Contemporary H5N1 Influenza Virus with an Expanded Host Range.
Discussion: In addition to the most often-observed substitution of E627K, there are several other important mutations in the PB2 protein, such as E158G, D253N, T271A, K526R, Q591K, A588V, D701N and so on, and these mutations had been proved to enhance polymerase activity.
Low Polymerase Activity Attributed to PA Drives the Acquisition of the PB2 E627K Mutation of H7N9 Avian Influenza Virus in Mammals.
Introduction: Different mutations in PB2 have been identified to contribute to the adaptation of influenza viruses to mammalian hosts; these mutations include E627K, D701N, T271A, Q591R/K, and E158G.
Dynamic Variation and Reversion in the Signature Amino Acids of H7N9 Virus During Human Infection.
PMID: 29688498
2018
The Journal of infectious diseases
Result: The D256G, T271A, M535L, Q591K, and H357N mutations were not detected in these samples (Supplementary Table 1).
Multiple polymerase gene mutations for human adaptation occurring in Asian H5N1 influenza virus clinical isolates.
Introduction: Other mutations in PB2, PB1 and PA also influence the host range of influenza viruses; e.g., PB2-D701N, PB2-K526R, PB2-Q591K, PB2-E192K and -K702R, PB2-I147T/K399T/A588T, PB2-E158G, PB1-L13P/S678N, PB1-
IV mutation literature information.
PMID: 
2021
Frontiers in cellular and infection microbiology
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