Abstract
Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is an accessory protein that interacts with a number of cellular and viral proteins. The functions of many of these interactions in the pathogenesis of HIV-1 have been identified. Deletion of the vpr gene reduces the virulence of HIV-1 dramatically, indicating the importance of this protein for the virus. This review describes the current findings on several established functions of HIV-1 Vpr and some possible roles proposed for this protein. Because Vpr exploits cellular proteins and pathways to influence the biology of HIV-1, understanding the functions of Vpr usually involves the study of cellular pathways. Several functions of Vpr are attributed to the virion-incorporated protein, but some of them are attributed to the expression of Vpr in HIV-1-infected cells. The structure of Vpr may be key to understanding the variety of its interactions. Due to the critical role of Vpr in HIV-1 pathogenicity, study of the interactions between Vpr and cellular proteins may help us to understand the mechanism(s) of HIV-1 pathogenicity.
Highlights
The virulence of a virus depends on the virus–host interactions, which are postulated by a variety of factors, such as route of virus entry, dose of the virus and the host’s age, sex, immune status and species
Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) enhances the ability of HIV-1 to replicate in terminally differentiated macrophages, which is attributed to the activity of Vpr in active nuclear import of the virus pre-integration complex (PIC) (Jenkins et al, 1998; Le Rouzic et al, 2002; Schang, 2003; Suzuki et al, 2009)
One hypothesis suggests that Vpr possesses structural features similar to those of HSP70, a cellular chaperone, enabling Vpr to bind to many proteins with sufficient energy to cause changes in the activity of target proteins (Basanez & Zimmerberg, 2001)
Summary
The virulence of a virus depends on the virus–host interactions, which are postulated by a variety of factors, such as route of virus entry, dose of the virus and the host’s age, sex, immune status and species. Some of the functions proposed for this protein include modulation of transcription of the virus genome (Sawaya et al, 2000), induction of apoptosis, disruption of cell-cycle control, induction of defects in mitosis (Chang et al, 2004), nuclear transport of the HIV-1 pre-integration complex (PIC) (Vodicka et al, 1998), facilitation of reverse transcription (Rogel et al, 1995), suppression of immune activation (Ramanathan et al, 2002) and reduction of the HIV mutation rate (Jowett et al, 1999). The cytopathic effects induced by Vpr are mostly attributed to the N terminus, which is able to form ion channels in cell membranes These effects are unrelated to the reported activities of Vpr, including virion association, G2 arrest, induction of apoptosis, etc. Alterations in the cell cycle, including apoptosis, cell-cycle arrest and defects in mitosis, are mostly carried out by the C-terminal domain of Vpr, alterations in the cell cycle by the other regions of Vpr have been reported (Piller et al, 1999; Roumier et al, 2002; Srinivasan et al, 2008)
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