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Int. J. Mol. Sci. 2017, 18(1), 126; doi:10.3390/ijms18010126

The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention

Unidad de Expresión Viral, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Carretera de Majadahonda-Pozuelo Km 2, Majadahonda, 28220 Madrid, Spain
Academic Editor: Brian Wigdahl
Received: 28 October 2016 / Revised: 22 December 2016 / Accepted: 3 January 2017 / Published: 10 January 2017
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Abstract

The human immunodeficiency virus type 1 (HIV-1) Vpr protein is an attractive target for antiretroviral drug development. The conservation both of the structure along virus evolution and the amino acid sequence in viral isolates from patients underlines the importance of Vpr for the establishment and progression of HIV-1 disease. While its contribution to virus replication in dividing and non-dividing cells and to the pathogenesis of HIV-1 in many different cell types, both extracellular and intracellular forms, have been extensively studied, its precise mechanism of action nevertheless remains enigmatic. The present review discusses how the apparently multifaceted interplay between Vpr and host cells may be due to the impairment of basic metabolic pathways. Vpr protein modifies host cell energy metabolism, oxidative status, and proteasome function, all of which are likely conditioned by the concentration and multimerization of the protein. The characterization of Vpr domains along with new laboratory tools for the assessment of their function has become increasingly relevant in recent years. With these advances, it is conceivable that drug discovery efforts involving Vpr-targeted antiretrovirals will experience substantial growth in the coming years. View Full-Text
Keywords: Vpr protein; mechanism of action; pathogenesis; cellular metabolism; antiretroviral target Vpr protein; mechanism of action; pathogenesis; cellular metabolism; antiretroviral target
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González, M.E. The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention. Int. J. Mol. Sci. 2017, 18, 126.

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