Mutation detail:
| Mutation site | S162N |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | HA |
| Gene ID | 23308115 |
| Country | Russia |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | clade 6B |
| 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 | 26992820 |
| Clinical information | No |
| Disease | - |
| Published year | 2016 |
| Journal | Influenza Other Respir Viruses |
| Title | Rapid spread of influenza A(H1N1)pdm09 viruses with a new set of specific mutations in the internal genes in the beginning of 2015/2024 epidemic season in Moscow and Saint Petersburg (Russian Federation) |
| Author | Andrey Komissarov,Artem Fadeev,Maria Sergeeva,Sergey Petrov,Kseniya Sintsova |
| Evidence | Figure 3 |