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HIV-1 Vpr increases Env expression by preventing Env from endoplasmic reticulum-associated protein degradation (ERAD).
- Source :
-
Virology . Sep2016, Vol. 496, p194-202. 9p. - Publication Year :
- 2016
-
Abstract
- Vpr enhances HIV-1 replication in macrophages and dendritic cells, as well as the human CD4 + CEM.NKR T cell line. Recently, Vpr was reported to increase HIV-1 Env expression in macrophages. Here, we report that Vpr also increases HIV-1 Env expression in dendritic cells and CEM.NKR cells. The Vpr activity depends on its N-terminal region, which was disrupted by a single A30L mutation. Env was rapidly degraded in the absence of Vpr, which was blocked by the ERAD pathway inhibitor kifunesine or the lysosome inhibitor Bafilomycin. As 2 O 3 or PK11195, which reportedly enhances HIV-1 Env folding, also blocked the Env degradation in CEM.NKR cells. Thus, these results not only identify Env as a primary target for Vpr to boost HIV-1 replication, but also suggest that Vpr likely promotes Env folding in the ER, which is otherwise misfolded and targeted by the ERAD pathway to lysosomes for degradation. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00426822
- Volume :
- 496
- Database :
- Academic Search Index
- Journal :
- Virology
- Publication Type :
- Academic Journal
- Accession number :
- 117095487
- Full Text :
- https://doi.org/10.1016/j.virol.2016.06.002