Journal article
Defining the roles for Vpr in HIV-1-associated neuropathogenesis
Journal of neurovirology, v 22(4), pp 403-415
Aug 2016
PMID: 27056720
Featured in Collection : UN Sustainable Development Goals @ Drexel
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.
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Details
- Title
- Defining the roles for Vpr in HIV-1-associated neuropathogenesis
- Creators
- Tony James - Department of Microbiology and Immunology, and Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Mail stop 1013-A, 245 N. 15th Street, Philadelphia, PA, 19102, USAMichael R Nonnemacher - Department of Microbiology and Immunology, and Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Mail stop 1013-A, 245 N. 15th Street, Philadelphia, PA, 19102, USABrian Wigdahl - Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USAFred C Krebs - Department of Microbiology and Immunology, and Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Mail stop 1013-A, 245 N. 15th Street, Philadelphia, PA, 19102, USA. fred.krebs@drexelmed.edu
- Publication Details
- Journal of neurovirology, v 22(4), pp 403-415
- Publisher
- Springer Nature; United States
- Grant note
- R01 DA019807 / NIDA NIH HHS R01 NS046263 / NINDS NIH HHS P30 MH092177 / NIMH NIH HHS R01 NS032092 / NINDS NIH HHS R01 NS089435 / NINDS NIH HHS T32 MH079785 / NIMH NIH HHS
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology
- Web of Science ID
- WOS:000378995700001
- Scopus ID
- 2-s2.0-84964053812
- Other Identifier
- 991014878210304721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences
- Virology