作者: Ge Li , Michael Bukrinsky , Richard Zhao
DOI: 10.2174/157016209787581436
关键词:
摘要: Human immunodeficiency virus type 1 (HIV-1) is engaged in dynamic and antagonistic interactions with host cells. Once infected by HIV-1, cells initiate various antiviral strategies, such as innate defense mechanisms, to counteract viral invasion. In contrast, the has different strategies suppress these responses infection. The final balance between determines outcome of infection disease progression. Recent findings suggest that HIV-1 protein R (Vpr) interacts some factors, heat shock proteins, plays an active role a pathogenic factor. Cellular stress response factors Vpr activities inhibit HIV replication. However, overcomes heat-stress-like preventing factor-1 (HSF-1) - mediated activation proteins. this review, we will focus on virus-host involving Vpr. addition discuss other EF2 Skp1/GSK3, their involvements cellular Vpr, well develop novel therapies aimed at enhancing anti-Vpr cell.