Journal
JOURNAL OF NEUROVIROLOGY
Volume 22, Issue 4, Pages 403-415Publisher
SPRINGER
DOI: 10.1007/s13365-016-0436-5
Keywords
HIV-1; Vpr; Neuropathogenesis; Brain; Exosome
Categories
Funding
- Comprehensive NeuroAIDS Center (CNAC) [P30 MH092177]
- Public Health Service, National Institutes of Health through National Institute of Neurological Disorders and Stroke [NS32092, NS46263, NS089435]
- Public Health Service, National Institutes of Health through National Institute of Drug Abuse [DA19807]
- Public Health Service, National Institutes of Health through National Institute of Mental Health under the Ruth L. Kirschstein National Research Service Award [5T32MH079785]
- Department of Microbiology and Immunology
- Institute for Molecular Medicine and Infectious Disease
- CNAC
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It is increasingly evident that the human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) has a unique role in neuropathogenesis. Its ability to induce G(2)/M arrest coupled with its capacity to increase viral gene transcription gives it a unique role in sustaining viral replication and aiding in the establishment and maintenance of a systemic infection. The requirement of Vpr for HIV-1 infection and replication in cells of monocytic origin (a key lineage of cells involved in HIV-1 neuroinvasion) suggests an important role in establishing and sustaining infection in the central nervous system (CNS). Contributions of Vpr to neuropathogenesis can be expanded further through (i) naturally occurring HIV-1 sequence variation that results in functionally divergent Vpr variants; (ii) the dual activities of Vpr as a intracellular protein delivered and expressed during HIV-1 infection and as an extracellular protein that can act on neighboring, uninfected cells; (iii) cell type-dependent consequences of Vpr expression and exposure, including cell cycle arrest, metabolic dysregulation, and cytotoxicity; and (iv) the effects of Vpr on exosome-based intercellular communication in the CNS. Revealing that the effects of this pleiotropic viral protein is an essential part of a greater understanding of HIV-1-associated pathogenesis and potential approaches to treating and preventing disease caused by HIV-1 infection.
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