AVM v1, released 02-OCT-22

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

Mutation detail:


Mutation site Q208K
Virus Influenzavirus A H1N1
Mutation level Amino acid Level
Gene/protein/region type M1
Gene ID 23308107
Country Russia
Mutation type nonsynonymous mutation
Genotype/subtype/clade -
Sample Human
Variants -
Viral reference sequence NC_026436.1
Drug/antibody/vaccine -
Transmissibility -
Transmission mechanism -
Pathogenicity -
Pathogenicity mechanism -
Immune escape mutation -
Immune escape mechanism -
RT-PCR primers probes -

Protein detail:


Protein name Matrix Protein 1
Uniprot protein ID C3W5X4
Protein length 252 amino acids
Protein description The M1 protein is composed of nine a-helices (H1-H9). These α-helices are organized into two four-helix bundles: N-terminal domain (H1-H4) and C terminal domain (H6-H9) connected via another helix linker (H5). The M1 protein plays critical roles in virus replication, from virus entry and uncoating to assembly and budding of the virus particle. M1 binding to ribonucleocapsids (RNPs) in nucleus seems to inhibit viral transcription. Interaction of viral NEP with M1-RNP is thought to promote nuclear export of the complex, which is targeted to the virion assembly site at the apical plasma membrane in polarized epithelial cells. Interactions with NA and HA may bring M1, a non-raft-associated protein, into lipid rafts. Forms a continuous shell on the inner side of the lipid bilayer in virion, where it binds the RNP. During virus entry into cell, the M2 ion channel acidifies the internal virion core, inducing M1 dissociation from the RNP. M1-free RNPs are transported to the nucleus, where viral transcription and replication can take place.

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 2015/2020 epidemic season in Moscow and Saint Petersburg (Russian Federation)
Author Andrey Komissarov,Artem Fadeev,Maria Sergeeva,Sergey Petrov,Kseniya Sintsova
Evidence Whole-genome analysis revealed a composition of specific mutations in the internal genes (D2E and M83I in NEP, E125D in NS1, M105T in NP, Q208K in M1, and N204S in PA-X) that probably emerged before the beginning of 2015/2020 epidemic season.