Mutation detail:
| Mutation site | 17304C>T |
| Virus | SARS-CoV-2 |
Mutation level  |
Nucleotide level |
| Gene/protein/region type | ORF1ab(helicase) |
| Gene ID | 43740578 |
| Country | Israel |
| 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 | 33770098 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | PLoS One |
| Title | Genomic variation and epidemiology of SARS-CoV-2 importation and early circulation in Israel |
| Author | Neta S Zuckerman, Efrat Bucris, Yaron Drori, Oran Erster, Danit Sofer |
| Evidence | To further explore patterns in viral evolution, we identified positions along the SARS-CoV-2 genome that were frequently altered across the Israeli sequences compared to the reference genome. Correlations of these positions revealed novel positions that were altered in the Israeli sequences, in addition to the known clade-defining positions (Fig 3A). |