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.
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.
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.
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.).
The effect of mutations derived from mouse-adapted H3N2 seasonal influenza A virus to pathogenicity and host adaptation.
Introduction: Furthermore, the E627K and D701N substitutions in the PB2 gene have been commonly detected in mouse-adapted IAVs and related to enhanced virulence in mice.
Amino acid substitutions involved in the adaptation of a novel H7N7 avian influenza virus in mice.
PMID: 32200160
2020
Research in veterinary science
Abstract: Genomic analysis of the mouse-adapted virus revealed amino acid changes in the PB2 (E525G, M645I, and D701N), NP (I475V), HA(D103N), and NA(K142E) proteins.
Detection of H3N8 influenza A virus with multiple mammalian-adaptive mutations in a rescued Grey seal (Halichoerus grypus) pup.
Abstract: From examining the protein alignments, we found several residue changes in the seal virus that did not occur in the bird viruses, including D701N in the PB2 segment, a rare mutation, and a hallmark of mammalian adaptation of bird viruses.
Result: Many of these changes occur in the polymerase complex genes: D701N in the PB2 segment is a rare mutation, and a hallmark of mammalian adaptation of bird influenza viruses, regardless of genetic background.
Result: We compared all the substitutions with previously described mutations in seal influenza virus infections, and found that apart from D701N, which was also found in the H3N8 seal virus infection in Massachusetts in 2011, there were no convergent amino acid changes.
Table:
Genetic and antigenic characterization of influenza A/H5N1 viruses isolated from patients in Indonesia, 2008-2015.
Result: PB2 substitutions such as E627K and D701N can dramatically increase polymerase activity of avian influenza viruses in mammalian cell
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.
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.
Genetic Characterization of a Novel North American-Origin Avian Influenza A (H6N5) Virus Isolated from Bean Goose of South Korea in 2018.
Discussion: According to the molecular analysis of gene segments between K6 and A/aquatic bird/Korea/CN5/2009 (H6N5), the D701N mutation in PB2 may contribute to the increased virulence observed for H6N5 in the mammalian host (Table 2).
Discussion: Particularly, the PB2 and/or PA gene of the CN5-2009 strain harboring D701N and L653P substitutions, respectively, can become reassorted with other K6 genes, resulting in potentially increased virulence in mammals.
PA Mutations Inherited during Viral Evolution Act Cooperatively To Increase Replication of Contemporary H5N1 Influenza Virus with an Expanded Host Range.
IV mutation literature information.
PMID: 
2021
Transboundary and emerging diseases
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