Mutation detail:
| Mutation site | C95A |
| Virus | Varicella-Zoster virus |
Mutation level  |
Amino acid level |
| Gene/protein/region type | ORF67 |
| Gene ID | 1487689 |
| Country | - |
| Mutation type |
nonsynonymous mutation |
| Genotype/subtype/clade | - |
| Sample |
cell line |
| Variants | - |
| Viral reference sequence | AB097933.1 |
| Drug/antibody/vaccine | - |
| Transmissibility |
- |
| Transmission mechanism | - |
| Pathogenicity |
decrease |
| Pathogenicity mechanism | - |
| Immune escape mutation | - |
| Immune escape mechanism | - |
| RT-PCR primers probes | - |
Protein detail:
| Protein name | Envelope Glycoprotein I |
| Uniprot protein ID | P09258 |
| Protein length | 354 amino acids |
| Protein description | 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 | 21345964 |
| Clinical information | No |
| Disease | - |
| Published year | 2011 |
| Journal | JOURNAL OF VIROLOGY |
| Title | Mutagenesis of Varicella-Zoster Virus Glycoprotein I (gI) Identifies a Cysteine Residue Critical for gE/gI Heterodimer Formation, gI Structure, and Virulence in Skin Cells |
| Author | Stefan L. Oliver,Marvin H. Sommer,Mike Reichelt,Jaya Rajamani,Leonssia Vlaycheva-Beisheim |
| Evidence | The gI C95A mutant failed to penetrate into the dermal layer of skin xenografts. Confocal microscopy of skin implants infected with rOka and the gI C95A, C106A, N116A, and del105-125 mutants |