| Virus Name | Venezuelan equine encephalitis |
| Virus Short Name | VEEV |
| Order | Unassigned |
| Virus Family | Togaviridae |
| Virus Subfamily | N.A. |
| Genus | Alphavirus |
| Species | Venezuelan equine encephalitis |
| Host | Human, mammals,mosquitoes and birds |
| Cell Tropism | N.A. |
| Associated Disease | Venezuelan equine encephalitis or encephalomyelitis (vee ) |
| Mode of Transmission | By infected mosquito |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_allSpecies_search.spg?method=SubmitForm&decorator=toga |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/positive-sense-rna-viruses-2011/w/posrna_viruses/275/togaviridae |
| Virus Host DB link | N.A. |
| Paper Title | siRNA Screen Identifies Trafficking Host Factors that Modulate Alphavirus Infection |
| Author's Name | Sheli R. Radoshitzky, Gianluca Pegoraro, Xiaoli Chi, Lian Dong, Chih-Yuan Chiang, Lucas Jozwick, Jeremiah C. Clester, Christopher L. Cooper, Duane Courier, David P. Langan, Knashka Underwood, Kathleen A. Kuehl, Mei G. Sun, Yi?ngyun Cai, Shuiqing Yu, Robin Burk, Rouzbeh Zamani, Krishna Kota, Jens H. Kuhn, Sina Bavari |
| Journal Name | PLoS Pathogens |
| Pubmed ID | 27031835 |
| Abstract | Little is known about the repertoire of cellular factors involved in the replication of pathogenic alphaviruses. To uncover molecular regulators of alphavirus infection, and to identify candidate drug targets, we performed a high-content imaging-based siRNA screen. We revealed an actin-remodeling pathway involving Rac1, PIP5K1- alpha, and Arp3, as essential for infection by pathogenic alphaviruses. Infection causes cellular actin rearrangements into large bundles of actin filaments termed actin foci. Actin foci are generated late in infection concomitantly with alphavirus envelope (E2) expression and are dependent on the activities of Rac1 and Arp3. E2 associates with actin in alphavirus-infected cells and co-localizes with Rac1-PIP5K1-alpha along actin filaments in the context of actin foci. Finally, Rac1, Arp3, and actin polymerization inhibitors interfere with E2 trafficking from the trans-Golgi network to the cell surface, suggesting a plausible model in which transport of E2 to the cell surface is mediated via Rac1- and Arp3-dependent actin remodeling. |
| Used Model | HeLa cells |
| DOI | 10.1371/journal.ppat.1005466 |
