Mutation detail:
| Mutation site | K229R |
| 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 | GQ166655.1 |
| Drug/antibody/vaccine | favipiravir resistant |
| Transmissibility |
promote |
| 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 | 34061908 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | PLoS Pathog |
| Title | Favipiravir-resistant influenza A virus shows potential for transmission |
| Author | Daniel H Goldhill,Ada Yan,Rebecca Frise,Jie Zhou,Jennifer Shelley |
| Evidence | Modelling revealed that due to a fitness advantage for the PA P653L mutant, reassortment with the wild-type virus to gain wild-type PB1 segment in vivo resulted in the loss of the PB1 resistance mutation K229R. |