Mutation detail:
| Mutation site | S206T |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | HA |
| Gene ID | 23308115 |
| Country | Mexico |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
Human |
| Variants | - |
| Viral reference sequence | NC_026433.1 |
| Drug/antibody/vaccine | adamantane resistant |
| 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 | 19465683 |
| Clinical information | No |
| Disease | - |
| Published year | 2009 |
| Journal | Science |
| Title | Antigenic and Genetic Characteristics of the Early Isolates of Swine-Origin 2009 A(H1N1) Influenza Viruses Circulating in Humans |
| Author | Rebecca J. Garten,C. Todd Davis,Colin A. Russell,Bo Shu,Stephen Lindstrom |
| Evidence | Analysis across the genomes of the 2009 A(H1N1) viruses from Mexico and the USA to date, found five minor genome variants: (i) the consensus sequence, (ii) T373I mutation in the NP paired with M582L mutation in the PA, (iii) amino acid substitutions of V106I and N247D in the NA (N2 numbering) paired with V100I in the NP and (iv) amino acid substitutions of S206T in the HA1 (H3 numbering) clustering with both V106I and N247D in the NA (N2 numbering), V100I in the NP and I123V in the NS1, and (v) amino acid substitutions of S91P, V323I (H3 numbering) together with S224P in the PA (Table S2). |