Mutation detail:
| Mutation site | L3201P |
| Virus | SARS-CoV-2 |
Mutation level  |
Amino acid level |
| Gene/protein/region type | ORF1ab(NSP4) |
| Gene ID | 43740578 |
| Country | Peru |
| 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 | 34704780 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | Microbiology spectrum |
| Title | The Emergence of Sars-CoV-2 Variant Lambda (C.37) in South America |
| Author | Pedro E Romero, Alejandra Davila-Barclay, Guillermo Salvatierra, Luis Gonzalez, Diego Cuicapuza |
| Evidence | C.37 contains a novel deletion (S: del 246 to 252, located at the N-terminal domain) plus seven nonsynonymous mutations in the Spike gene (G75V, T76I, D253N, L452Q, F490S, D614G, T859N) (Fig. 1C). Mutations L452Q and F490S both map to the Spike proteins receptor-binding domain (RBD). While L452Q is almost exclusive to C.37, L452R is present in variant of concern (VOC) delta (B.1.617.2) and variants of interest (VOI) epsilon (B.1.427/B.1.429) and kappa (B.1.617.1) and is associated with increased affinity for the ACE2 receptor (2). F490S has been associated with reduced in vitro susceptibility to antibody neutralization (3, 4). C.37 also displays the ORF1a del 3675 to 3677 deletion, found in VOCs alpha, beta, and gamma (5). |