IV mutation literature information.


  V292I mutation in PB2 polymerase induces increased effects of E627K on influenza H7N9 virus replication in cells.
 PMID: 25409547       2014       Nature communications
Abstract: Here we show that mutation PB2-K526R is present in some human H7N9 influenza isolates, in nearly 80% of H5N1 human isolates from Indonesia and, in conjunction with E627K, in almost all seasonal H3N2 viruses since 1970.
Abstract: Host-adaptive strategies, such as the E627K substitution in the PB2 protein, are critical for replication of avian influenza A viruses in mammalian hosts.
Discussion: The PB2 E627K substitution is recognized as a dominant adaptation marker in the majority of human-adapted influenza A viruses, facilitating replication in mammalian cells, however, the 590S/591R motif was found to complement the function of 627K in the PB2 of 2009 H1N1 virus to allow replication i


  Multiple amino acid substitutions involved in the adaptation of H6N1 avian influenza virus in mice.
 PMID: 25457364       2014       Veterinary microbiology
Abstract: Sequencing of the variants revealed amino acid changes in the PB2 (E627K), PA (T97I), and HA (N394T) proteins.


  Investigation of influenza virus polymerase activity in pig cells.
 PMID: 23077313       2013       Journal of virology
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.


  Unstable polymerase-nucleoprotein interaction is not responsible for avian influenza virus polymerase restriction in human cells.
 PMID: 23115299       2013       Journal of virology
Abstract: Avian-origin influenza virus polymerase activity can be dramatically increased in human cells with the PB2 E627K mutation.
Abstract: However, we demonstrate here that a variety of PB2 adaptive mutations, including E627K, do not enhance the stability of the vRNP but rather increase the amount of replicated RNA that results in more PB2-NP coprecipitation.


  Molecular and serological investigations of the Influenza A(H1N1) 2009 pandemic virus in Turkey.
 PMID: 23483248       2013       Medical microbiology and immunology
Abstract: Thirteen rRT-PCR positive samples were analyzed for presence of mutations that have been associated with host range, virulence, and antiviral resistance: substitution D222G in the HA, E627K in the PB2, and H275Y in the neuraminidase (NA).


  Molecular detection of human H7N9 influenza A virus causing outbreaks in China.
 PMID: 23665848       2013       Clinical chemistry
Abstract: The virus is a reassortant of avian viruses, but these human isolates contain mutations [hemagglutinin (HA) Q226L and PB2 E627K] that might make it easier for the virus to adapt to mammalian hosts.


  Asparagine substitution at PB2 residue 701 enhances the replication, pathogenicity, and transmission of the 2009 pandemic H1N1 influenza A virus.
 PMID: 23799150       2013       PloS one
Abstract: The 2009/2010 pandemic influenza virus (H1N1pdm) contains an avian-lineage PB2 gene that lacks E627K and D701N substitutions important in the pathogenesis and transmission of avian-origin viruses in humans or other mammals.
Result: Although the increased RNA polymerase activity conferred by PB2-D701N was fairly modest in comparison to other mutations (e.g., E627K, and E158G), seemingly small differences in RNA polymerase activity may still influence transmission or pathogenesis.
Result: Mice inoculated with rNY1682-WT, rNY1682-E627K and rNY1682-D701N, began to lose weight by 3 dpi; and more significant weight loss was observed in the mice inoculated with rN


  Fecal influenza in mammals: selection of novel variants.
 PMID: 23966381       2013       Journal of virology
Abstract: Most of the novel genotypes emerged as PB2(E627K), HA(F128V), HA(F454L), or HA(H300P) variations, and double mutations frequently occurred in the same isolate.


  [Genomic sequences of human infection of avian-origin influenza A(H7N9)virus in Zhejiang province].
 PMID: 24125614       2013       Zhonghua liu xing bing xue za zhi
Abstract: The E627K mutation was shared by all the other novel H7N9 viruses resulted in human infections through analysis on the currently available sequences.
Abstract: The sequenced virus showed Q226L mutation in HA protein, but E627K was not presented in PB2 protein of this virus.
Abstract: The virus showed Q226L mutation on HA protein but E627K did not present on PB2 protein of this virus.


  Adaptation of novel H7N9 influenza A virus to human receptors.
 PMID: 24162312       2013       Scientific reports
Introduction: H7N9 viruses isolated from human possess for instance the E627K substitution in the PB2 RNA polymerase subunit, which has been shown to facilitate RNA replication in mammalian cells and transmission between ferrets.



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