Abstract: The MVV mutations caused no weight loss in mice, but they did allow replication in infected lungs, and the viruses acquired fatal mammalian pathogenic mutations such as Q591R/K, E627K, or D701N in the infected lungs.
Result: Cloned amplicons encoding amino acid residues 590-701 were sequenced, and well-known mammalian pathogenic mutations such as Q591R/K, E627K, and D701N were identified in four out of five lungs.
Result: Surprisingly, at least half of the quasi-species of three mice possessed mammalian pathogenic mutations (Q591K, E627K, or D701N), and double mutations [E627K (10/10) and
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.
H9N2 Influenza A Virus Isolated from a Greater White-Fronted Wild Goose (Anser albifrons) in Alaska Has a Mutation in the PB2 Gene, Which Is Associated with Pathogenicity in Human Pandemic 2009 H1N1.
Introduction: demonstrated that the introduction of a point mutation (Q591K) increased polymerase activity and allowed the virus to replicate in human cells.
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.
Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses.
Method: Site-directed mutagenesis was performed using pFLAG-CMV5.1-H7N9-PB2 to generate -K627E, -V139I&K627E, -K191E&K627E, -V511I&K627E, -M535L&K627E, -N559T&K627E, -M570I&K627E, -Q591K&K627E, -I647V&K627E, -M676V&K627E, and -D701N&
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.
PB2 segment promotes high-pathogenicity of H5N1 avian influenza viruses in mice.
Discussion: In addition, mutation Gln591Lys of PB2 could compensate for the lack of PB2-627Lys and increase the virulence of an avian H5N1 influenza virus in mice (Yamada et al.,).
Discussion: The results support the contribution of the virus without 627Lys or 701Asn or Gln591Lys could be compensated for by other mutations at other sites of PB2.
The K526R substitution in viral protein PB2 enhances the effects of E627K on influenza virus replication.
Abstract: In addition, minimal combinations of three (PB2 Q236H, E627K, and NP N309K) or two (PB2 Q591K and NP S50G) mutations were sufficient to recapitulate the efficient growth in HTBE cells of dk/AB/76 viruses isolated after 10 passages in this substrate.
Abstract: The results indicate that coupling of the mammalian-adaptive mutation PB2 E627K or Q591K to selected mutations in NP further augments the growth of the corresponding viruses.
IV mutation literature information.
PMID: 
2017
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