| Virus Name | Vesicular stomatitis Indiana virus |
| Virus Short Name | VSV |
| Order | Mononegavirales |
| Virus Family | Rhabdoviridae |
| Virus Subfamily | N.A. |
| Genus | Vesiculovirus |
| Species | Indiana vesiculovirus |
| Host | Human, cattle, horse, swine, sandflies, blackflies |
| Cell Tropism | N.A. |
| Associated Disease | Vesicular diseases, encephalitis |
| Mode of Transmission | Mostely by sandflies |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_allSpecies_search.spg?method=SubmitForm&decorator=rhabdo |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/negative-sense-rna-viruses-2011/w/negrna_viruses/201/rhabdoviridae |
| Virus Host DB link | N.A. |
| Paper Title | Endoplasmic reticulum chaperone gp96 is essential for infection with vesicular stomatitis virus |
| Author's Name | Stuart Bloor, Jonathan Maelfait, Rebekka Krumbach, Rudi Beyaert and Felix Randow |
| Journal Name | PNAS |
| Pubmed ID | 20351288 |
| Abstract | The envelope glycoprotein of vesicular stomatitis virus (VSV-G) enables viral entry into hosts as distant as insects and vertebrates. Because of its ability to support infection of most, if not all, human cell types VSV-G is used in viral vectors for gene therapy. However, neither the receptor nor any specific host factor for VSV-G has been identified. Here we demonstrate that infection with VSV and innate immunity via Toll-like receptors (TLRs) require a shared component, the endoplasmic reticulum chaperone gp96. Cells without gp96 or with catalytically inactive gp96 do not bind VSV-G. The ubiquitous expression of gp96 is therefore essential for the remarkably broad tropism of VSV-G. Cells deficient in gp96 also lack functional TLRs, which suggests that pathogen-driven pressure for TLR-mediated immunity maintains the broad host range of VSV-G by positively selecting for the ubiquitous expression of gp96. |
| Used Model | N.A. |
| DOI | 10.1073/pnas.0908536107 |
