AVM v1, released 02-OCT-22

A manually curated database of aerosol-transmitted virus mutations, human diseases, and drugs

Mutation detail:


Mutation site S203T
Virus Influenzavirus A H1N1
Mutation level Amino acid Level
Gene/protein/region type HA
Gene ID 23308115
Country Japan
Mutation type nonsynonymous mutation
Genotype/subtype/clade clade 7
Sample Human
Variants -
Viral reference sequence NC_026434.1
Drug/antibody/vaccine -
Transmissibility -
Transmission mechanism -
Pathogenicity -
Pathogenicity mechanism -
Immune escape mutation -
Immune escape mechanism -
RT-PCR primers probes -

Protein detail:


Protein name Hemagglutinin
Uniprot protein ID C3W627
Protein length 566 amino acids
Protein description The HA protein is translated as an uncleaved HA0 precursor protein, folded as a trimer, and glycosylated and acylated. The HA protein binds to sialic acid-containing receptors on the cell surface, bringing about the attachment of the virus particle to the cell. This attachment induces virion internalization either through clathrin-dependent endocytosis or through clathrin- and caveolin-independent pathway. Plays a major role in the determination of host range restriction and virulence. Class I viral fusion protein. Responsible for penetration of the virus into the cell cytoplasm by mediating the fusion of the membrane of the endocytosed virus particle with the endosomal membrane. Low pH in endosomes induces an irreversible conformational change in HA2, releasing the fusion hydrophobic peptide. Several trimers are required to form a competent fusion pore.

Literature information:


Pubmed ID 24078044
Clinical information No
Disease -
Published year 2013
Journal virus genes
Title Molecular evolution of the hemagglutinin and neuraminidase genes of pandemic (H1N1) 2009 influenza viruses in Sendai, Japan, during 2009-2011
Author Irona Khandaker,Akira Suzuki,Taro Kamigaki,Kentaro Tohma,Takashi Odagiri
Evidence Phylogenetic tree analysis demonstrated that Sendai isolates were clustered into global clade 7, which is characterized by an S203T mutation in the HA1 gene. Moreover, two distinct circulation clusters were present in the 2010-2011 season. Mutations were present in antigenic or receptor-binding domains of the HA1 segment, including A141V, S143G, S183P, S185T, and S203T