Abstract: Since 2006, several reports of IAV isolations from emus have surfaced and avian influenza infection of emus can lead to the selection of mammalian like PB2-E627K and PB2-D701N mutants.
Genomic Signatures for Avian H7N9 Viruses Adapting to Humans.
Abstract: An RNP activity assay showed that Q591K, D701N, and M535L restored the polymerase activity in human cells when 627K transformed to an avian-like E.
Abstract: An RNP assay suggested Q591K, D701N, and M535L as potential markers for an H7N9 virus capable of infecting humans.
Introduction: Other PB2 mutations including Q591K, and D701N were also investigated for their enhancing polymerase activity in human 293T cells.
Introduction: Three genetic substitutions, PB2 E627K, D701
PB2-588 V promotes the mammalian adaptation of H10N8, H7N9 and H9N2 avian influenza viruses.
Introduction: Another well-known substitution D701N in PB2 is primarily found in a duck
Discussion: Many adaptive mutations in PB2, such as E627K, D701N, K526R, and T271A have been proven to be important for different avian influenza viruses to break the host species barrier to infect mammals.
Discussion: Previous studies have shown that D701N and E627K may influence the interaction of PB2 with different isoforms of importin-alpha to adapt mammalian hosts and a recent study showed that the PB2-627K resists the signaling-independent antiviral effect of RIG-I by increasing nucleocapsid stability.
Amino acid changes in PB2 and HA affect the growth of a recombinant influenza virus expressing a fluorescent reporter protein.
Result: In fact, the PB2-D701N and PB2-S714R mutations facilitate adaptation of avian influenza viruses to mammals by affecting the PB2 interaction with importin, resulting in better exposure of the PB2 nuclear localization signal.
Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses.
Method: Furthermore, a mouse infection study was performed after observing no increase in progeny vRNA production of the selected viruses carrying mutations compared to previously published studies, and the PB2-D701N mutant virus was excluded from the in vivo mouse infection study although this mutant showed reduced progeny vRNA production in human cells compared to EG/D1 (wt) virus.
Method: In this study, all the mutations introduced into recombinant EG/D1 virus (clade 2.2.1) were naturally detected as single/multiple intra-segment mutations or inter-segment combinations of the mutations in clade 2.2.1 viruses isolated from patients, except artificial mutation PB2-D701N.
Result: In this study, PB2-D701N was included as a reference mutation, although this human adaptation
Detection of reassortant avian influenza A (H11N9) virus in environmental samples from live poultry markets in China.
PMID: 27268229
2016
Infectious diseases of poverty
Table: D701N
Susceptibility and Status of Avian Influenza in Ostriches.
Abstract: Seventeen of 27 (63%) ostrich viruses contained the polymerase basic 2 (PB2) E627K marker, and 2 of the ostrich isolates that lacked E627K contained the compensatory Q591K mutation, whereas a third virus had a D701N mutation.
Amino acid substitutions involved in the adaptation of a novel highly pathogenic H5N2 avian influenza virus in mice.
Result: Several amino acid substitutions including PB2 (Q591K and D701N), polymerase acidic protein (PA) (I554V), HA (S227N), and NP (R351K) have been described in mouse adapted H5N2 AIVs that have increased virulence and enhanced replication kinetics in mice and cell lines.
PB2 E627K or D701N substitution does not change the virulence of canine influenza virus H3N2 in mice and dogs.
Introduction: As residues at positions 627 and 701 of the polymerase basic protein 2 (PB2) are considered critical for the mammalian adaptation of avian influenza viruses, several studies have independently shown that single E627K (glutamic acid to lysine) or D701N (aspartic acid to asparagine) mutations could increase polymerase activity and viral replication in mammalian cells and the pathogenicity of H7N9 viruses in the BALB/c mouse model.
Introduction: Our findings show that both the E627K and D701N mutations occurred in ferrets that had direct contact with infected animals within a few days post-exposure.
Introduction: Yet it is still unknown whether spontaneous emergence of dual D701N and E627K mutations can occur readily in infecte
Adaptive mutations in PB2 gene contribute to the high virulence of a natural reassortant H5N2 avian influenza virus in mice.
Abstract: Genomic sequencing revealed five mutations (HA-S227N, PB2-Q591K, PB2-D701N, PA-I554V and NP-R351K) that distinguished HB10-MA virus from its parental HB10 virus.
Abstract: Therefore, our results collectively emphasized the crucial role of PB2 gene, particularly the paired mutations of Q591K and D701N in the host adaptation of the novel reassortant H5N2 AIV in mammals, which may provide helpful insights into the pathogenic potential of emerging AIV in human beings.
IV mutation literature information.
PMID: 
2017
Virology
Browser Board
Co-occurred Entities
Filtrator
ViMRT