Mutation detail:
| Mutation site | K279R |
| 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 | LC333183.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
- |
| 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 | 31068418 |
| Clinical information | No |
| Disease | - |
| Published year | 2019 |
| Journal | JOURNAL OF VIROLOGY |
| Title | Single-Cell Virus Sequencing of Influenza Infections That Trigger Innate Immunity |
| Author | Alistair B. Russell,Elizaveta Elshina,Jacob R. Kowalsky,Aartjan J. W. te Velthuis,Jesse D. Bloom |
| Evidence | The strongest IFN induction was by the NS1stop virus, but the PB1 internal deletion and three of the point mutant viruses (PB1-D27N, PB1-T677A, and NS1-A122V) also induced IFN significantly more frequently than the wild type. The other three point mutants (PB1-G206S, PB1-K279R, and NS2-E47G) did not increase IFN induction, an unsurprising finding since we expected some mutations without an IFN-enhancing effect to be found in IFN+cells by chance. |