Pathogenesis and genetic characteristics of a novel reassortant low pathogenic avian influenza A(H7N6) virus isolated in Cambodia in 2019.
PMID: 34347386
2021
Transboundary and emerging diseases
Abstract: Although avian-origin A(H7Nx) LPAIVs do not contain the critical mammalian-adaptive substitution (E627K) in PB2, the lethality and morbidity of the A(H7N6) virus in BALB/c mice were similar to those of A(H7N9) viruses, suggesting potential for interspecies transmission.
Mutations during the adaptation of H7N9 avian influenza virus to mice lungs enhance human-like sialic acid binding activity and virulence in mice.
Abstract: Sequence analysis showed that the two viruses differed by 27 amino acids distributed among six genes, containing changes in PB2 (E627K, D701N) and HA (Q226L) genes.
Characterization of the low-pathogenic H7N7 avian influenza virus in Shanghai, China.
Discussion: In this study, no key amino acid mutations were found in PB2, especially the E627 K and D701 N mutations, which have been shown to increase adaptation of other AIVs to mammals.
The PB2 co-adaptation of H10N8 avian influenza virus increases the pathogenicity to chickens and mice.
PMID: 34008327
2021
Transboundary and emerging diseases
Abstract: Several well-known adaptive mutations in the PB2 gene, such as E627K, D701N, and A588V, significantly enhanced the virulence of the AIVs in mammals.
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
Abstract: More importantly, after 5 passages in mice, the virus acquired two adaptive mutations, PB1-H115Q and B2-E627K, exhibiting increased virulence and aerosol transmissibility.
Introduction: reported that mutations in PB2 (E627K), NA (R294K) and PA (V100A) were significantly correlated with increased mortality, while other mutations in HA (N276D) and PB2 (N559T) were distinctly correlated with mild cases.
Result: The sequence analysis revealed that two amino acid substitutions in the MA-P5 virus, one in the PMID: 34061017
2021
The Journal of general virology
Abstract: K526R, E627V or E627K), indicating a host adaptation advantage for these double mutations.
Genetic and antigenic characterization of influenza A/H5N1 viruses isolated from patients in Indonesia, 2008-2015.
Result: Both PB2-E627K (5 of 35 viruses) and PB2-D701N (1 virus) substitutions were observed in a limited number of the novel viruses presented in this study.
Result: In particular, PB2-E627K is a key molecular determinant of host range and a virulence factor during human infection with
Discussion: Although some genetic diversity was observed in the polymerase genes, well-known substitutions such as PB2-E627K and PB2-D701N, which are often selected upon infection of humans and affects the virulence of avian influenza viruses such as H5N1, were not commonly found in the new samples.
Effect of the selection pressure of vaccine antibodies on evolution of H9N2 avian influenza virus in chickens.
Discussion: Mutation on the RNP complex will increase the infectivity and host range of influenza viruses, such as 588V, E627K, G685R and D701N on PB2 (Song et al.; Wei and Liu; Xiao et al.; Zhang et al.).
Reassortment and adaptive mutations of an emerging avian influenza virus H7N4 subtype in China.
Abstract: Mutations in PB2 (E627K), PB2 (K683T), PB1-F2 (N47S), HA (N283D), HA(K321E), NA(A137V), NA(K296R) and M2 (C19Y) were identified in the human isolate while no mutations were found in PB1, Discussion: Second, E627K in PB2 of the human H7N4 virus may have been a determinant of host range.
Mutations in PB2 and HA enhanced pathogenicity of H4N6 avian influenza virus in mice.
PMID: 31081750
2020
The Journal of general virology
Abstract: Further studies showed that the introduction of E158K and/or E627K substitutions into PB2 significantly increased polymerase activity, which led to the enhanced replication and virulence of BJ21-MA.
Abstract: Molecular analysis of BJ21-MA identified four mutations, located in proteins PB2 (E158K and E627K) and HA (L331I and G453R, H3 numbering).