Abstract

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

Keywords: HIV-1, Vpr, host cellular responses, viral pathogenesis, heat shock factors, EF2, Skp1/GSK3, host-pathogen interaction