Mutation detail:
Mutation site | T566A |
Virus | Influenzavirus A H1N1 |
Mutation level ![]() |
Amino acid Level |
Gene/protein/region type | PB1 |
Gene ID | 23308122 |
Country | China |
Mutation type ![]() |
nonsynonymous mutation |
Genotype/subtype/clade | - |
Sample ![]() |
cell line |
Variants | - |
Viral reference sequence | GQ166227.1 |
Drug/antibody/vaccine | - |
Transmissibility ![]() |
- |
Transmission mechanism | - |
Pathogenicity ![]() |
increase |
Pathogenicity mechanism | - |
Immune escape mutation | - |
Immune escape mechanism | - |
RT-PCR primers probes | - |
Protein detail:
Protein name | Polymerase PB1 |
Uniprot protein ID | C3W5X7 |
Protein length | 757 amino acids |
Protein description | RNA-dependent RNA polymerase which is responsible for replication and transcription of virus RNA segments. The transcription of viral mRNAs occurs by a unique mechanism called cap-snatching. 5' methylated caps of cellular mRNAs are cleaved after 10-13 nucleotides by PA. In turn, these short capped RNAs are used as primers by PB1 for transcription of viral mRNAs. During virus replication, PB1 initiates RNA synthesis and copy vRNA into complementary RNA (cRNA) which in turn serves as a template for the production of more vRNAs |
Literature information:
Pubmed ID | 21698272 |
Clinical information | No |
Disease | - |
Published year | 2011 |
Journal | PLoS One |
Title | Genomic Polymorphism of the Pandemic A (H1N1) Influenza Viruses Correlates with Viral Replication, Virulence, and Pathogenicity In Vitro and In Vivo |
Author | Lili Xu,Linlin Bao,Jianfang Zhou,Dayan Wang,Wei Deng |
Evidence | These mutations led to amino acid substitutions in HA (L32I), PA (A343T), PB1 (K353R and T566A), and PB2 (T471M), and may be critical molecular determinants for replication, virulence, and pathogenicity. |