Special Issue "HIV Latency"

Guest Editor
Prof. Dr. Fatah Kashanchi
Director of Research, National Center for Biodefense and Infectious Diseases, Professor of Microbiology, George Mason University, Discovery Hall, Room 182, 10900 University Blvd. MS 1H8, Manassas, Va 20110
Website: http://researchfocus.gmu.edu/node/684
E-Mail: fkashanc@gmu.edu
Phone: +703 993 9160
Fax: +703 993 7022

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Type of Paper: Article
Title: Lost in Transcription: molecular mechanisms that control HIV latency
Authors: Ran Taube ^1# and Matija Peterlin ² 
Affiliations: ¹ The Shraga Segal Department of Microbiology Immunology and Genetics;  ² Department of Medicine, University of California, San Francisco, CA 94143,  USA; ^# To whom correspondence should be addressed: Ran Taube, Ph.D., The Shraga Segal Department of, Microbiology Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer-Sheva, ISRAEL 84105, Phone: 972-8-6479858, Fax: 972-8-6479953, email: rantaube@bgu.ac.il
Abstract: Highly Active Antiretroviral Therapy (HAART) has limited the replication and spread of Human Immunodeficiency Virus (HIV). However, despite treatment, HIV infection persists in early-established latently infected reservoirs and once therapy is interrupted viral replication quickly rebounds. Extensive efforts are being directed at eliminating these reservoirs by reactivating latent HIV while administering drugs that prevent new rounds of infection and allow for the clearance of infected cells by the immune system. However, current approaches to eradicate HIV have not been effective and the significance of each of the molecular mechanisms that drive HIV into latency is still under debate. The establishment of HIV latency is multifactorial, where transcriptional repression plays a significant role. Among the pathways that increase latency, reduced levels and activity of the Positive Transcription Elongation Factor b (CDK9/cyclin T; P-TEFb) is crucial, thus increasing its expression and activity is an excellent strategy to reactivate viral gene expression.From the virus point of view, this review summarizes the multiple mechanisms that cause HIV to enter latency. It positions the interplay between transcriptionally active and inactive host transcriptional activators and their viral partner Tat as valid targets for the development of new strategies that aim to reactivate latent viral gene expression and completely eradicate HIV.
Keywords: HIV latency; transcriptional interference; epigenetic; Tat; Positive Transcription elongation factor b (P-TEFb)

Type of Paper: Article
Title: Induced Degradation of Tat by NC via the Proteasome Pathway and Its Effect on HIV Transcription
Authors: Hye-Won Hong¹, Seong-Wook Lee², and Heejoon Myung^1,*
Affiliations: ¹ Department of Bioscience and Biotechnology, Hankuk University of Foreign Studies, Yong-In, Gyung-Gi Do, Korea; E-Mails: hehe-wow@hanmail.net (H-W.H.); hjmyung@hufs.ac.kr (H.M.); ² Department of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, Yong-In, Gyung-Gi Do, Korea; E-Mail: swl0208@dankook.ac.kr; * Author to whom correspondence should be addressed; E-Mail: hjmyung@hufs.ac.kr; Tel.: +82-31-330-4098; Fax: +82-31-330-4566.
Abstract: Human Immunodeficiency Virus type 1 (HIV-1) is a retrovirus that causes acquired immunodeficiency syndrome (AIDS). HIV-1 Tat protein upregulates transcriptional transactivation. The nucleocapsid protein NC of HIV-1 is a component of virion and plays a key role in genome packaging. Herein, we have demonstrated the interaction between NC and Tat by means of a yeast two-hybrid assay, GST pull-down analysis, co-immunoprecipitation and subcellular colocalization analysis. We observed that the level of Tat was significantly reduced in the presence of NC. But NC did not affect mRNA expression level of Tat. The level of Tat in the presence of NC was increased by treating cells with a proteasome inhibitor, MG132. The ubiquitination state of Tat was not seen to increase in the presence of NC, suggesting the proteasomal degradation was independent of ubiquitination. Lowered level of Tat in the presence of NC led to a decrease in Tat-mediated transcriptional transactivation.
Keywords: Human immunodeficiency virus (HIV); nucleocapsid (NC); Tat; proteasomal degradation