Discussion: The D225G and NAg+F2P associations with increased pathogenicity or symptoms appeared after a pandemic and after an antigenic drift event that each led to viral population dominance by a single genotype and its descendants.
Discussion: Within human H1N1 viruses, recent pandemic strains with the HA mutation D225G associated with infection of the lower airways, likely due to the increased binding of alpha2,3-linked sialic acid, and increased disease.
Genetic sequencing of influenza A (H1N1) pdm09 isolates from South India, collected between 2011 and 2015 to detect mutations affecting virulence and resistance to oseltamivir.
PMID: 33154243
2020
Indian journal of medical microbiology
Abstract: Two samples collected from expired patients had D239N (D222G or D225G) mutation in HA.
Genetic diversity of influenza A viruses circulating in Bulgaria during the 2018-2019 winter season.
PMID: 32459617
2020
Journal of medical microbiology
Result: Of the three egg-adaptation substitutions in the A/Singapore/INFIMH-16-0019/2016 vaccine virus (T160K resulting in the loss of a glycosylation sequon in antigenic site B, L194P in the 190-helix (residues 188-194) and D225G within the RBS), one Bulgarian virus (A/Bulgaria/1153/2019) carried T160K substitution and two (A/Bulgaria/1534/2018 and A/Bulgaria/900/2019) showed polymorphism at this position (T160X).
Identification of Key Amino Acids in the PB2 and M1 Proteins of H7N9 Influenza Virus That Affect Its Transmission in Guinea Pigs.
Introduction: reported that two amino acid mutations, D190E and D225G, abolished the ability of the 1918/H1N1 virus to transmit via respiratory droplets between ferrets.
Complete genome sequencing of H1N1pdm09 swine influenza isolates from Nigeria reveals likely reverse zoonotic transmission at the human-animal interface in intensive piggery.
Discussion: Though the observation of host-induced selection of variants was reported for Q226R or D225G of earlier human H1N1pdm09 viruses, this study observed Q240R substitution.
Amino Acid Substitutions HA A150V, PA A343T, and PB2 E627K Increase the Virulence of H5N6 Influenza Virus in Mice.
Introduction: Receptor binding preference is a crucial component in adaption, pathogenicity, and transmission (citation updated and moved to backward), with only a few substitutions, for instance, HA D190E, D225G, Q192H, and K193R, influenza virus can change receptor specificity, from avian type to human type.
[Mutations in Hemagglutinin and Polymerase Alter the Virulence of Pandemic A(H1N1) Influenza Virus].
Abstract: Thus, (1) substitutions in HA (Asp225Gly or Gln226Arg) and compensatory mutation decreasing the charge of HA (Lys123Asn, Lys157Asn, Gly158Glu, Asn159Asp, or Lys212Met) altered viral receptor-binding specificity and restored the functional balance between HA and NA; (2) Phe35Leu substitution in the PA protein increased viral polymerase activity.
A Single-Amino-Acid Substitution at Position 225 in Hemagglutinin Alters the Transmissibility of Eurasian Avian-Like H1N1 Swine Influenza Virus in Guinea Pigs.
Introduction: reported that a 2-amino-acid change, D190E and D225G, in the viral hemagglutinin (HA) protein abolishes the transmission of 1918/H1N1 influenza virus in ferrets.
Discussion: Two amino acid mutations, D190E and D225G, abolished the ability of the 1918/H1N1 virus to transmit via respiratory droplet between ferrets.
A reassortant H9N2 influenza virus containing 2009 pandemic H1N1 internal-protein genes acquired enhanced pig-to-pig transmission after serial passages in swine.
Result: the substitution of aspartic acid by glycine at position 225 of the Discussion: Although specific receptor-binding tests would be necessary to elucidate the exact role of the HA-D225G mutation within the HA-RBS, our data suggest that it may be a marker for adaptation of H9N2 viruses to swine.
Discussion: Regarding the mutations detected during the analysis, only one of the mutations that appeared in the virus after seven passages and was maintained even after transmission, the HA-D225G substitution in the RBS.
Discussion: The presence of the HA-D225G mutation after seven passages may therefore explain the consistent replication in the lungs during passage eight.