Mutation detail:
| Mutation site | N6301S |
| Virus | SARS-CoV-2 |
Mutation level  |
Amino acid level |
| Gene/protein/region type | ORF1ab(3'-to-5' exonuclease) |
| Gene ID | 43740578 |
| Country | Japan |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
Human |
| Variants | - |
| Viral reference sequence | NC_045512.2 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
- |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | ORF1ab polyprotein |
| Uniprot protein ID | P0DTC1 |
| Protein length | 7096 amino acids |
| Protein description | ORF1ab, the largest gene, contains overlapping open reading frames that encode polyproteins PP1ab and PP1a. The polyproteins are cleaved to yield 16 nonstructural proteins, NSP1-16. Production of the longer (PP1ab) or shorter protein (PP1a) depends on a -1 ribosomal frameshifting event. The proteins, based on similarity to other coronaviruses, include the papain-like proteinase protein (NSP3), 3C-like proteinase (NSP5), RNA-dependent RNA polymerase (NSP12, RdRp), helicase (NSP13, HEL), endoRNAse (NSP15), 2'-O-Ribose-Methyltransferase (NSP16) and other nonstructural proteins. SARS-CoV-2 nonstructural proteins are responsible for viral transcription, replication, proteolytic processing, suppression of host immune responses and suppression of host gene expression. The RNA-dependent RNA polymerase is a target of antiviral therapies. |
Literature information:
| Pubmed ID | 34097716 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | PLoS Pathogens |
| Title | Detection of R.1 lineage severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with spike protein W152L/E484K/G769V mutations in Japan |
| Author | Yosuke Hirotsu,Masao Omata |
| Evidence | Our sequencing analysis of the SARS-CoV-2 isolates from the three family members identified the same 21 mutations in each isolate; these comprised 13 missense, six synonymous, and two intergenic variants. Among the missense mutations, four were in the spike protein (W152L, E484K, D614G, and G769V), four were in ORF1ab (T4692I, N6301S, L6337M, and I6525T), one was in the membrane protein (F28L), and four were in the nucleocapsid protein (S187L, R203K, G204R, and Q418H). |