AVM v1, released 02-OCT-22

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

Mutation detail:


Mutation site D86Y
Virus Influenzavirus A H1N1
Mutation level Amino acid Level
Gene/protein/region type HA
Gene ID 23308115
Country China
Mutation type nonsynonymous mutation
Genotype/subtype/clade Clade 7
Sample Human
Variants -
Viral reference sequence NC_026433.1
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 27515172
Clinical information No
Disease -
Published year 2016
Journal Original Article
Title Dynamic patterns of circulating influenza virus from 2005 to 2012 in Shandong Province, China
Author Ti Liu, Zhong Li, Yi Lin, Shaoxia Song, Shengyang Zhang,
Evidence The HA phylogeny shows that the amino acid substitutions P83S, S203 and I321V were found in all of the Shandong isolates.The substitutions S128P and D86G/Y were identified in 50 % and 30 % of the A/H1N1 pdm09 viruses in the 2009-2010 and 2010-2011 season, respectively.