Mutation detail:
| Mutation site | N66S |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | PB1 |
| Gene ID | 23308122 |
| Country | - |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | CY010378.1 |
| 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 | 22318139 |
| Clinical information | No |
| Disease | - |
| Published year | 2012 |
| Journal | JOURNAL OF VIROLOGY |
| Title | PB1-F2 modulates early host responses but does not affect the pathogenesis of H1N1 seasonal influenza virus |
| Author | Isabelle Meunier,Veronika von Messling |
| Evidence | An early delay in innate immune activation has been observed in lung tissues of mice infected with a sublethal mouse-adapted virus carrying the PB1-F2 N66S mutation (3), supporting a growing body of evidence from in vitro studies that PB1-F2 delays innate immune activation (5, 30). |