Abstract
The HIV-1 Vpr protein is a viral accessory protein that plays a number of important roles during HIV infection. The activities of Vpr are numerous and include the induction of apoptosis, the modulation of cell cycle arrest, as well as control of viral transcription. Study of HIV clones lacking Vpr in vitro and analysis of HIV variants isolated from longterm nonprogressors in vivo highlight the importance of Vpr for viral replication as well as immune suppression and cell death. Vpr may therefore be considered among the most important accessory proteins encoded by HIV.
Keywords: HIV-1, viral protein R (Vpr), viral transcription, apoptosis, cell cycle arrest, mitochondrial membrane potential and immune suppression
Current HIV Research
Title: HIV-1 Vpr: Regulator of Viral Survival
Volume: 7 Issue: 2
Author(s): Khanh P. Thieu, Matthew P. Morrow, Devon J. Shedlock, Kimberly A. Schoenly, Karthikbabu Mallilankaraman, Andrew Y. Choo, Paolo Fagone, David B. Weiner and Karuppiah Muthumani
Affiliation:
Keywords: HIV-1, viral protein R (Vpr), viral transcription, apoptosis, cell cycle arrest, mitochondrial membrane potential and immune suppression
Abstract: The HIV-1 Vpr protein is a viral accessory protein that plays a number of important roles during HIV infection. The activities of Vpr are numerous and include the induction of apoptosis, the modulation of cell cycle arrest, as well as control of viral transcription. Study of HIV clones lacking Vpr in vitro and analysis of HIV variants isolated from longterm nonprogressors in vivo highlight the importance of Vpr for viral replication as well as immune suppression and cell death. Vpr may therefore be considered among the most important accessory proteins encoded by HIV.
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Cite this article as:
Thieu P. Khanh, Morrow P. Matthew, Shedlock J. Devon, Schoenly A. Kimberly, Mallilankaraman Karthikbabu, Choo Y. Andrew, Fagone Paolo, Weiner B. David and Muthumani Karuppiah, HIV-1 Vpr: Regulator of Viral Survival, Current HIV Research 2009; 7 (2) . https://dx.doi.org/10.2174/157016209787581454
DOI https://dx.doi.org/10.2174/157016209787581454 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
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