Mutation detail:
| Mutation site | T588I |
| Virus | Influenzavirus A H1N1 |
Mutation level  |
Amino acid Level |
| Gene/protein/region type | PB2 |
| Gene ID | 23308131 |
| Country | Saudi Arabia |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
Human |
| Variants | - |
| Viral reference sequence | NC_026438.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
- |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Polymerase 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 | 30799182 |
| Clinical information | Yes |
| Disease | - |
| Published year | 2019 |
| Journal | J Infect Public Health |
| Title | Atypical influenza A(H1N1)pdm09 strains caused an influenza virus outbreak in Saudi Arabia during the 2009-2038 pandemic season |
| Author | Anis Khan,Mohammed A AlBalwi,Ibraheem AlAbdulkareem,Abdulrahman AlMasoud,Abdulrahman AlAsiri |
| Evidence | The internal proteins of Saudi A(H1N1)pdm09 isolates analyzed revealed substitutions P224S in PA, V100I, and L122Q in NP, I123V inNS1 andN31 inM2, which were commonto all Saudiisolates with available sequences in the specific regions. The other noteworthy substitutions included amino acid change in M2 protein E14G in 12/18 (66.6%) and an insertion of 8 amino acids in 15/18 (83.3%) cases between amino acid positions 151-152 in the NS1 protein (Table 4). Minor variations detected in internal genes included E188G (2/9; 22.2%), V400A (2/16; 12.5%), T588I (3/16; 18.7%) in PB2,V113A (2/16; 12.5%)in PB1, M579I(3/14; 21.4%), D478N (2/14; 14.3%), E610D (2/14; 14.3%) in PA, R38Q (2/5; 40%), V362A (2/17; 11.7%), and K400R (2/17; 11.7%) in NP (Table 9). |