Mutation detail:
| Mutation site | del27549-27644 |
| Virus | SARS-CoV-2 |
Mutation level  |
Nucleotide level |
| Gene/protein/region type | ORF7a |
| Gene ID | 43740573 |
| Country | - |
| Mutation type |
- |
| Genotype/subtype/clade | - |
| Sample |
Human |
| Variants | - |
| Viral reference sequence | NC_045512.2 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
decrease |
| Pathogenicity mechanism | We isolate one of these mutant viruses from a patient sample and use viral challenge experiments to link this isolate (ORF7a-del115) to a growth defect. ORF7a is implicated in immune modulation, and we show that the C-terminal truncation negates anti-immu |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | ORF7a protein |
| Uniprot protein ID | P0DTC7 |
| Protein length | 121 amino acids |
| Protein description | The orf 7a of SARS-CoV-2 is a transmembrane protein with four regions from the N-terminal: 1) the first 15 amino acids form a signal peptide which is hydrolyzed by the infected host cells; 2) the amino acids from 16 to 96 constitute the intracellular domain; 3) the 97- 117 amino acids are hydrophobic amino acids constituting a transmembrane domain; and 4) the last five amino acids constitute the C- terminal of the orf7a. The orf7a interacts with the S, M, E, and the orf3a proteins, which suggest a role of the protein in the assembling of the virus and in the binding and invasion of the virus to the host cells. |
Literature information:
| Pubmed ID | 34043946 |
| Clinical information | No |
| Disease | - |
| Published year | 2021 |
| Journal | Cell Reports |
| Title | SARS-CoV-2 genomic surveillance identifies naturally occurring truncation of ORF7a that limits immune suppression |
| Author | Artem Nemudryi, Anna Nemudraia, Tanner Wiegand, Joseph Nichols, Deann T Snyder |
| Evidence | Using global phylogenomics, we show that mutations frequently occur in the C-terminal end of ORF7a. We isolate one of these mutant viruses from a patient sample and use viral challenge experiments to link this isolate (ORF7a-del115) to a growth defect |