Abstract: Two amino acid substitutions, T128D and N139K, located in the head domain of the H2 hemagglutinin (HA) molecule, were identified as important determinants of antigenic change during A/H2N2 virus evolution.
[Genetic characteristic of hemagglutinin of avian influenza A (H7N9) virus in Guizhou Province in 2017].
PMID: 30744302
2019
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
Abstract: Mutation G186V at the receptor binding sites in the HA was found in all 14 strains, and mutation Q226L in 13 strains besides A/Guizhou-Weining/CSY01/2017.
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Abstract: Characterization of a pandemic 2009 H1N1 influenza virus isolated from a fatal case patient (F-IAV), showed the presence of three different mutations; potential determinants of its high pathogenicity that were located in the polymerase subunits (PB2 A221T and PA D529N) and the hemagglutinin (HA S110L).
Abstract: Here, we have evaluated the contribution of HA S110L to F-IAV pathogenicity, through introduction of this point mutation in CAL recombinant virus (HA mut).
Abstract: In addition, recombinant viruses containing HA S110L
Molecular evolution of influenza B virus during 2011-2017 in Chaoyang, Beijing, suggesting the free influenza vaccine policy.
Abstract: Substitutions L58P, I146V were observed in HA1 region of Victoria-lineage virus in 2011-2012 and I117V, N129D were showed in 2015-2017.
Abstract: The amino acids substitutions of HA1 region were R279K in strains of 2011-2014 and L173Q, M252V in strains of 2014-2017.
Table: I117V
Table: I146V
Table: N116K
Table: N129D
Discussion: As expected, substitution N116K was key mutation in 2013-2015 seasons and caused Yamagata-lineage to be absolute prevalence.
Atypical influenza A(H1N1)pdm09 strains caused an influenza virus outbreak in Saudi Arabia during the 2009-2011 pandemic season.
PMID: 30799182
2019
Journal of infection and public health
Abstract: RESULTS: Concatenated whole-genome phylogenetic analysis along with hemagglutinin (HA) signature changes, that is, Aspartic Acid (D) at position 187, P83S, S203T, and R223Q confirmed that the Saudi strains belong to the antigenic category of A/California/07/2009.
Genetic diversity of influenza A(H3N2) viruses in Northern Cameroon during the 2014-2016 influenza seasons.
Abstract: Analysis of the coding regions of the NA and M genes showed that none had genetic markers of resistance to neuraminidase inhibitors but all strains possessed the S31N substitution of resistance to amantadine.
Evolved avian influenza virus (H7N9) isolated from human cases in a middle Yangtze River city in China, from February to April 2017.
Abstract: The hemagglutinin segment contained Thr160Ala, Gly186Val and Gln226Leu substitutions, which are associated with increased binding affinity in humans.
Abstract: The proportion of PB2 Ala588Val substitutions in viruses revealed a significantly increasing in recent years, from 0.8 % (1 of 128 cases) to 84.9 % (275 of 324 cases).
Result: A
Result: A number of H7N9 viruses had acquired Arg292Lys substitution associated with oseltamivir-resistance in NA gene until April 2017.
Result: Amantadine resistance was evident and the resistance-conferring mutation was identified as Ser31Asn in the M2 gene (Table 3).
The PB2 Polymerase Host Adaptation Substitutions Prime Avian Indonesia Sub Clade 2.1 H5N1 Viruses for Infecting Humans.
Result: Acquisition of the E627K substitution in PB2 following infection in humans or other mammalian hosts has been observed for avian H5N1, H7N7 and H7N9 viruses.
Result: Adaptation of E627K in PB2 was found to facilitate virus replication at a lower temperature in the upper respiratory tract.
Result: An adaptive E627K substitution in PB2 was found to enhance PB2 interaction with NP in the RNP complex.
Result: Analysis using a minigenome reporter assay indicated that R288Q is relevant to RNP polymerase activity.
Result: Apart from human cases infected with Qinghai-like vir
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Introduction: Antiviral susceptibilities of the polymerase acidic subunit protein I38T mutant viruses.
Introduction: Both PA I38T mutant viruses showed normal inhibition with all four NA inhibitors, but exhibited 49- and 68-fold higher IC50 values to baloxavir compared with the median IC50 value of A(H3N2) viruses isolated in the 2018/19 influenza season in Japan.
Introduction: Deep sequencing analysis of the isolates using MiSeq (Illumina, San Diego, California, United States) revealed that A/YOKOHAMA/87/2019 and A/YOKOHAMA/88/2019 possessed the PA I38T substitution.
Introduction: Detection of polymerase acidic subunit I38T mutant influenza A(H3N2)
Positive charge of Arg-201 on hemagglutinin is required for the binding of H6N1 avian influenza virus to its target through a two-step process.
Abstract: We found that the positive charge on R201 was critical for binding HA to the negatively charged surface of host cells because the mutant R201A of H6HA0 lost its binding capacity substantially.
IV mutation literature information.
PMID: 
2019
Journal of virology
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