Mutation detail:
| Mutation site | E111Q |
| Virus | Varicella-Zoster virus |
Mutation level  |
Amino acid level |
| Gene/protein/region type | ORF68 |
| Gene ID | 1487709 |
| Country | - |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
Human |
| Variants | - |
| Viral reference sequence | AB097933.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
- |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Envelope Glycoprotein E |
| Uniprot protein ID | P09259 |
| Protein length | 623 amino acids |
| Protein description | Envelope glycoprotein that binds to the potential host cell entry receptor IDE. In epithelial cells, the heterodimer gE/gI is required for the cell-to-cell spread of the virus, by sorting nascent virions to cell junctions. Once the virus reaches the cell junctions, virus particles can spread to adjacent cells extremely rapidly through interactions with cellular receptors that accumulate at these junctions. Implicated in basolateral spread in polarized cells. In neuronal cells, gE/gI is essential for the anterograde spread of the infection throughout the host nervous system. Together with US9, the heterodimer gE/gI is involved in the sorting and transport of viral structural components toward axon tips |
Literature information:
| Pubmed ID | 20593027 |
| Clinical information | No |
| Disease | - |
| Published year | 2010 |
| Journal | Plos One |
| Title | Insulin Degrading Enzyme Induces a Conformational Change in Varicella-Zoster Virus gE, and Enhances Virus Infectivity and Stability |
| Author | Qingxue Li,Mir A Ali,Kening Wang,Dean Sayre,Frederick G Hamel |
| Evidence | Mutation of glutamic acid 111 to glutamine in IDE results in a mutant protein, IDE-E111Q, which is catalytically inactive for insulin degradation. |