Mutation detail:
| Mutation site | L366I |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | PA |
| Gene ID | 23308128 |
| Country | - |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | M23974.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
promote |
| Transmission mechanism | and the resultant virus (rFluMist/pH1N1-P20_PA-I366L) replicated more efficiently in mouse lungs and caused greater weight loss than rFluMist/pH1N1-P20 (Fig. 5). In total, |
| Pathogenicity |
- |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Polymerase PA |
| Uniprot protein ID | C3W5X6 |
| Protein length | 716 amino acids |
| Protein description | PA Plays an essential role in viral RNA transcription and replication by forming the heterotrimeric polymerase complex together with PB1 and PB2 subunits. The complex transcribes viral mRNAs by using a unique mechanism called cap-snatching. It consists in the hijacking and cleavage of host capped pre-mRNAs. These short capped RNAs are then used as primers for viral mRNAs. The PB2 subunit is responsible for the binding of the 5' cap of cellular pre-mRNAs which are subsequently cleaved after 10-13 nucleotides by the PA subunit that carries the endonuclease activity. |
Literature information:
| Pubmed ID | 27440882 |
| Clinical information | No |
| Disease | - |
| Published year | 2016 |
| Journal | J Virol |
| Title | Reversion of Cold-Adapted Live Attenuated Influenza Vaccine into a Pathogenic Virus |
| Author | Bin Zhou,Victoria A Meliopoulos,Wei Wang,Xudong Lin,Karla M Stucker |
| Evidence | Sequencing of the variant identified seven nonsynonymous mutations, PB1-E51K, PB1-I171V, PA-N350K, PA-L366I, NP-N125Y, NP-V186I, and NS2-G63E. |