AVM v1, released 02-OCT-22

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

Mutation detail:


Mutation site T588I
Virus Influenzavirus A H1N1
Mutation level Amino acid Level
Gene/protein/region type PB2
Gene ID 23308131
Country -
Mutation type nonsynonymous mutation
Genotype/subtype/clade -
Sample cell line
Variants -
Viral reference sequence GQ149617.1
Drug/antibody/vaccine -
Transmissibility -
Transmission mechanism -
Pathogenicity increase
Pathogenicity mechanism These results indicate that early viral replication and higher virus titers contribute to the increased pathogenicity in mice.
Immune escape mutation -
Immune escape mechanism -
RT-PCR primers probes -

Protein detail:


Protein name Polymerase PB2
Uniprot protein ID C3W5X5
Protein length 759 amino acids
Protein description PB2 plays an essential role in transcription initiation and cap-stealing mechanism, in which cellular capped pre-mRNAs are used to generate primers for viral transcription. Recognizes and binds the 7-methylguanosine-containing cap of the target pre-RNA which is subsequently cleaved after 10-13 nucleotides by the viral protein PA. Plays a role in the initiation of the viral genome replication and modulates the activity of the ribonucleoprotein (RNP) complex.

Literature information:


Pubmed ID 24335306
Clinical information No
Disease -
Published year 2014
Journal JOURNAL OF VIROLOGY
Title PB2-588I enhances 2009 H1N1 pandemic influenza virus virulence by increasing viral replication and exacerbating PB2 inhibition of beta interferon expression
Author Zongzheng Zhao,Chenyang Yi,Lianzhong Zhao,Shengyu Wang,Lishan Zhou
Evidence These findings indicate that the pdm/09 influenza virus has increased pathogenicity upon the acquisition of the PB2-T588I mutation and highlight the need for the continued surveillance of the genetic variation of molecular markers in influenza viruses because of their potential effects on pathogenicity and threats to human health.