Mutation detail:
| Mutation site | 10301C>A |
| Virus | SARS-CoV-2 |
Mutation level  |
Nucleotide level |
| Gene/protein/region type | ORF1ab(3C-like proteinase) |
| Gene ID | 43740578 |
| Country | France |
| Mutation type |
- |
| 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 | 33931941 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | EMBO Molecular Medicine |
| Title | SARS-CoV-2 worldwide replication drives rapid rise and selection of mutations across the viral genome: a time-course study-potential challenge for vaccines and therapies |
| Author | Stefanie Weber, Christina M Ramirez, Barbara Weiser, Harold Burger, Walter Doerfler |
| Evidence | We examined mutations in 383,570 complete sequences with known sampling dates in GISAID up until January 20, 2021. Figure 1 shows the worldwide distribution of Spike mutations as well as other variants of interest over time from April 2020 to March 31, 2021, from complete sequences with a known collection date deposited in GISAID. Table 1 lists the signature mutations for the variants. Table 2 shows the total number of complete sequences each variant of interest (B.1.1.7 (the UK variant), 501Y.V2 (the South African variant) and 484K.V2 (B.1.1 lineage with S: E484K/D614G, V1176F N: A199S/R203K/G204R) deposited in GISAID by each country as of March 31, 2021. |