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. |