Abstract

Publisher Summary This chapter describes the interactions of human immunodeficiency virus type 1(HIV‐1) viral protein R (Vpr) with host cell proteins. Active host–pathogen interactions take place during HIV‐1 infection of host cells. HIV‐infected cells respond to viral invasion with various antiviral strategies, such as innate, cellular, and humoral immune antiviral defense mechanisms, and the virus has developed tactics to suppress these host responses to infection. The final balance among these interactions determines the efficiency of the viral infection and subsequent disease progression. Some recent findings suggest that Vpr interacts with some of the host innate antiviral responses, such as heat stress responses, and plays an active role as a viral pathogenic factor; cellular heat stress response factors counteract such Vpr activities as nuclear import, the induction of cell cycle G2/M arrest, and the apoptosis of the host cells and also inhibit HIV replication. The chapter also discusses the other Vpr‐interacting proteins and their potential roles in HIV replication and strategies for the development of future antiviral therapies directed at suppressing Vpr activities.

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