Mutation detail:
| Mutation site | D701N |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | PB2 |
| Gene ID | 23308131 |
| Country | - |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | FJ966079.1 |
| 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 PB2 |
| Uniprot protein ID | C3W5X5 |
| Protein length | 759 amino acids |
| Protein description | PB2 plays an essential role in transcription initiation and cap-stealing mechanism, in which cellular capped pre-mRNAs are used to generate primers for viral transcription. Recognizes and binds the 7-methylguanosine-containing cap of the target pre-RNA which is subsequently cleaved after 10-13 nucleotides by the viral protein PA. Plays a role in the initiation of the viral genome replication and modulates the activity of the ribonucleoprotein (RNP) complex. |
Literature information:
| Pubmed ID | 20689744 |
| Clinical information | No |
| Disease | - |
| Published year | 2010 |
| Journal | MBIO |
| Title | The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase |
| Author | Brett W. Jagger,Matthew J. Memoli,Zong-Mei Sheng, a Li Qi,Rachel J. Hrabal,Genevieve L. Allen |
| Evidence | Next, the impact of the PB2-E627K (CA09RNP-E627K) and D701N (CA09RNP-D701N) mutations on viruses containing the 2009 pandemic RNP was assessed. Surprisingly, rather than increasing the growth of the CA09RNP virus, both of these mutant viruses grew to a 1- to 2-log-lower peak titer than the parental CA09RNP virus (P= 0.0058 and 0.0075, respectively). |