Mutation detail:
| Mutation site | 896A>G |
| Virus | Human respiratory syncytial virus |
Mutation level  |
Nucleotide Level |
| Gene/protein/region type | NS2 |
| Gene ID | 1494469 |
| Country | - |
| Mutation type |
- |
| Genotype/subtype/clade | A |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | AY911262.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
- |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Non-structural Protein 2 |
| Uniprot protein ID | P04543 |
| Protein length | 124 amino acids |
| Protein description | Non-structural Protein 2(NS2) plays a major role in antagonizing the type I IFN-mediated antiviral response. NS2 acts cooperatively with NS1 to repress activation and nuclear translocation of host IFN-regulatory factor IRF3. NS2 Interacts with the host cytoplasmic sensor of viral nucleic acids DDX58/RIG-I and prevents the interaction with its downstream partner MAVS. Together with NS2, participates in the proteasomal degradation of host STAT2, IRF3, IRF7, TBK1 and DDX58 through a NS-degradasome involving CUL2 and Elongin-C. The degradasome requires an intact mitochondrial MAVS. Induces host SOCS1 expression. Induces activation of NF-kappa-B. Suppresses premature apoptosis by an NF-kappa-B-dependent, interferon-independent mechanism promoting continued viral replication. |
Literature information:
| Pubmed ID | 33684421 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | Virus Research |
| Title | Steady-state persistence of respiratory syncytial virus in a macrophage-like cell line and sequence analysis of the persistent viral genome |
| Author | Ximena Ruiz-Gomez, Joel Armando Vazquez-Perez, Oscar Flores-Herrera, Mercedes Esparza-Perusquia, Carlos Santiago-Olivares |
| Evidence | Table 2 |