Mutation detail:
| Mutation site | S82I |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | M2 |
| Gene ID | 23308108 |
| Country | Ukraine |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | NC_026434.1 |
| Drug/antibody/vaccine | oseltamivir resistant |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
increase |
| Pathogenicity mechanism | Correspondingly, viruses harboring these NS1 mutations exhibited increased virulence in mouse models of influenza.Mutation N321K in PA occurred in all isolates and confers increased virulence [48]. The NP mutation M105T is in a motif under selective press |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Matrix Protein 2 |
| Uniprot protein ID | C3W5X3 |
| Protein length | 97 amino acids |
| Protein description | The M2 protein channel consists of 97 residues: (1) an ectodomain (residues 1-24); (2) the pore-forming TM helix (residues 25-43); (3) an amphiphilic C-terminal helix (residues 47-60); and (4)a cytoplasmic tail (residues 61-97). The influenza A virus M2 protein, a tetrameric type III integral transmembrane (TM) protein, is known to play an essential role in viral replication by mediating the acidification and uncoating of endosomally entrapped virus. The tetrameric M2 in the viral membrane functions as pH-dependent proton channels to equilibrate pH across the viral membrane during entry and across the trans-Golgi membrane of infected cells during viral maturation. |
Literature information:
| Pubmed ID | 34834932 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | Viruses |
| Title | Genotypic Variants of Pandemic H1N1 Influenza A Viruses Isolated from Severe Acute Respiratory Infections in Ukraine during the 2015/16 Influenza Season |
| Author | Oksana Zolotarova,Anna Fesenko,Olga Holubka,Larysa Radchenko,Eric Bortz |
| Evidence | For phylogenetic analysis, isolates were taken from the 2014/15 and 2015/16 epidemic seasons. All isolates including the A/California/07/2009 vaccine strain had the D21G mutation in the M2 protein (Figure 6), which causes resistance to antiviral drugs amantadine and rimantadine, which are ion channel inhibitors. A few isolates also contained unique point substitutions in the M2 protein (S23N, I28V, and S82I). |