| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3424222 | Virology | 2013 | 13 Pages |
Chikungunya virus (CHIKV) is a re-emerging alphavirus transmitted by Aedes mosquitoes. Infection with CHIKV elicits a type I interferon response that facilities virus clearance, probably through the action of down-stream effectors such as antiviral IFN-stimulated genes (ISGs). Bone marrow stromal antigen 2 (BST-2) is an ISG shown to restrict HIV-1 replication by preventing the infection of bystander cells by tethering progeny virions on the surface of infected cells. Here we show that enrichment of cell surface BST-2 results in retention of CHIKV virus like particles (VLPs) on the cell membrane. BST-2 was found to co-localize with CHIKV structural protein E1 in the context of VLPs without any noticeable effect on BST-2 level. However, CHIKV nonstructural protein 1 (nsP1) overcomes BST-2-mediated VLPs tethering by down-regulating BST-2 expression. We conclude that BST-2 tethers CHIKV VLPs on the host cell plasma membrane and identify CHIKV nsP1 as a novel BST-2 antagonist.
Graphical abstractFigure optionsDownload full-size imageDownload high-quality image (236 K)Download as PowerPoint slideHighlights► BST-2/tetherin retains CHIKV VLPs on the cell membrane. ► CHIKV structural (E1) and nonstructural proteins (nsP1) localizes with BST-2. ► BST-2 is in complex with E1 and nsP1. ► nsP1 but not E1 counteracts BST-2-mediated tethering of CHIKV VLPs. ► nsP1 but not E1 down-regulates BST-2 expression.
