IMR Press / FBL / Volume 9 / Issue 4 / DOI: 10.2741/1403

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Role of viral regulatory and accessory proteins in HIV-1 replication
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1 Department of Biochemistry and Molecular Biology, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20037
2 Department of Microbiology and Tropical Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20037
3 The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850
Front. Biosci. (Landmark Ed) 2004, 9(4), 2388–2413;
Published: 1 September 2004

Human immunodeficiency virus-1 (HIV-1) is the causative agent of acquired immune deficiency syndrome (AIDS), a disease characterized by CD4+ T lymphocyte depletion. HIV-1 replicates actively in a variety of cells by encoding several regulatory (Tat and Rev) and accessory (Vpr, Vif, Vpu, and Nef) proteins. Accessory proteins, thought initially to be dispensable for infection, have now been shown to be important for efficient infection in vivo. Recent evidence suggests that certain viral proteins, like Vif, have evolved to overcome the antiviral mechanisms of the host, while proteins like Nef, which are markers for disease pathogenesis in vivo, help to increase pathogenesis by targeting bystander cells. Thus, these proteins control many aspects of the virus life cycle as well as host cell function, namely gene regulation and apoptosis. Understanding the mechanisms by which the virus is able to successfully replicate in host cells and subsequently cause gradual destruction of the immune system may yield new approaches for therapeutic strategies. In this review, we attempt to integrate information on the role of these regulatory and accessory proteins, emphasizing their interactions with other viral and cellular components, and the subsequent effect on viral replication.

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