Abstract：
: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 G2/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.
journal_name
J Neuroviroljournal_title
Journal of neurovirologyauthors
James T,Nonnemacher MR,Wigdahl B,Krebs FCdoi
10.1007/s13365-016-0436-5subject
Has Abstractpub_date
2016-08-01 00:00:00pages
403-15issue
4eissn
1355-0284issn
1538-2443pii
10.1007/s13365-016-0436-5journal_volume
22pub_type
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journal_title：Journal of neurovirology
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journal_title：Journal of neurovirology
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journal_title：Journal of neurovirology
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