Abstract: We also investigated in pig cells the consequences of some known mammalian host range determinants that enhance influenza virus polymerase activity in human cells, such as PB2 mutations E627K, D701N, G590S/Q591R, and T271A.
Two mutations in the C-terminal domain of influenza virus RNA polymerase PB2 enhance transcription by enhancing cap-1 RNA binding activity.
Abstract: D701N and S714R mutations enhanced transcription by enhancing cap-1 RNA-binding activity, but they may exhibit decreased efficiency of priming by the cap-1 primer.
Abstract: Cap-1 RNA-binding activities of D701N/S714R, D701N, and S714R were 262+-25%, 257+-34%, and 315+-9.6% of that of the wt, respectively, and their cap-dependent endonuclease activities were similar to that of the wt.
Abstract: Cap-1-dependent transcription activities of D701N/S714R, D701N, and S714R were 348.1+-6.2%, 146.4+-11%, and 250.1+-0.8% of that of the wild type (wt), respectively.
Abstract: The mutant human influenza virus RdRp containing
H4N8 subtype avian influenza virus isolated from shorebirds contains a unique PB1 gene and causes severe respiratory disease in mice.
Introduction: However, point mutations of known molecular markers, such as PB2 E627K / D701N/ E677G, PB1-F2 N66S, and PA T97I, produced no significant change in pathogenicity when incorporated in pH1N1 individually.
Emergence of fatal avian influenza in New England harbor seals.
Abstract: These include a D701N mutation in the viral PB2 protein, previously reported in highly pathogenic H5N1 avian influenza viruses infecting people.
Result: The seal H3N8 virus from the 2011 outbreak has naturally acquired this D701N substitution (Table 1), which was confirmed by clonal sequencing directly from infected tissue (50 clones/animal) to be the only phenotype present in all five animals.
Result: This D701N mutation has been experimentally introduced into an adapted version of the H7N7 seal influenza virus isolated in 1982 (1, 2) and was shown to increase the pathogenicity of the virus to mice.
[Molecular characterization of highly pathogenic avian influenza A (H5N1) viruses isolated from humans in Hunan province, 2006 - 2009].
PMID: 21933546
2011
Zhonghua liu xing bing xue za zhi
Abstract: D701N mutation of PB2 that increased the virulence in mice was found in HN/1/08.
Comparative analysis of avian influenza virus diversity in poultry and humans during a highly pathogenic avian influenza A (H7N7) virus outbreak.
Abstract: These include the independent emergence of HA A143T mutants, accumulation of four NA mutations, and farm-to-farm spread of virus variants harboring mammalian host determinants D701N and S714I in PB2.
Influenza A virus NS1 gene mutations F103L and M106I increase replication and virulence.
Introduction: Key mutations in the PB2 gene increased pathogenicity and viral transmission such as E627K and D701N and mutation sites in H3 HA1 and HA2 subunits, G218W and T156N respectively, have been shown to affect both growth and virulence in the mouse.
Interaction of the influenza A virus polymerase PB2 C-terminal region with importin alpha isoforms provides insights into host adaptation and polymerase assembly.
PMID: 21216958
2011
The Journal of biological chemistry
Abstract: Two effects were observed: first, adaptive mutations D701N, R702K, and S714R in the nuclear localization signal domain increased 2-4-fold the association rates with avian and human importins; second, measurement of different structural forms of the PB2 C terminus demonstrated that the upstream 627 domain reduced binding affinity, consistent with a steric clash predicted from crystal structures.
PB2 and hemagglutinin mutations are major determinants of host range and virulence in mouse-adapted influenza A virus.
Abstract: In this study, we demonstrate that MA mutations of the PB2 (D701N) and hemagglutinin (HA) (G218W in HA1 and T156N in HA2) genes were the most adaptive genetic determinants for increased growth and virulence in the mouse model.
Abstract: Minigenome transcription assays showed that PB1 and PB2 mutations increased polymerase activity and that the PB2 D701N mutation was comparable in effect to the mammalian adaptive PB2 E627K mutation.
IV mutation literature information.
PMID: 
2013
Journal of virology
Browser Board
Co-occurred Entities
Filtrator
ViMRT