Special Issue "HIV Latency"
Deadline for manuscript submissions: closed (31 July 2014)
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
Phone: +703 993 9160
Fax: +703 993 7022
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed Open Access monthly journal published by MDPI.
Viruses 2013, 5(3), 902-927; doi:10.3390/v5030902
Received: 27 February 2013; in revised form: 15 March 2013 / Accepted: 18 March 2013 / Published: 21 March 2013| Cited by 8 | PDF Full-text (899 KB) | HTML Full-text
Article: Induced Degradation of Tat by Nucleocapsid (NC) via the Proteasome Pathway and Its Effect on HIV Transcription
Viruses 2013, 5(4), 1143-1152; doi:10.3390/v5041143
Received: 18 March 2013; in revised form: 16 April 2013 / Accepted: 16 April 2013 / Published: 23 April 2013| PDF Full-text (467 KB) | HTML Full-text | XML Full-text
Article: Quantifying Susceptibility of CD4+ Stem Memory T-Cells to Infection by Laboratory Adapted and Clinical HIV-1 Strains
Viruses 2014, 6(2), 709-726; doi:10.3390/v6020709
Received: 20 December 2013; in revised form: 5 February 2014 / Accepted: 6 February 2014 / Published: 10 February 2014| Cited by 1 | PDF Full-text (1421 KB) | HTML Full-text | XML Full-text
Viruses 2014, 6(4), 1715-1758; doi:10.3390/v6041715
Received: 2 January 2014; in revised form: 18 March 2014 / Accepted: 20 March 2014 / Published: 14 April 2014| PDF Full-text (2110 KB) | HTML Full-text | XML Full-text
Viruses 2014, 6(4), 1837-1860; doi:10.3390/v6041837
Received: 2 January 2014; in revised form: 11 March 2014 / Accepted: 28 March 2014 / Published: 22 April 2014| PDF Full-text (971 KB) | HTML Full-text | XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: HIV eradication: multiple approaches to activate viral replication
Author: Tokameh Mahmoudi
Affiliation: Associate Professor of Biochemistry, Erasmus University Medical Centre Ee634, Dr. Molewaterplein 50, 3015GE Rotterdam, The Netherlands
Abstract: The concept of eradication of the Human Immune Deficiency Virus (HIV) from infected patients has gained much attention in the last few years. While combination Anti-Retroviral Therapy (c-ART) has been extremely effective in suppressing viral replication, it is not curative. This is due to the presence of a reservoir of latent HIV infected cells, which are replication competent, and which persist in the presence of c-ART. Recently, pharmaceutical approaches have focused on the development, characterization and testing of molecules able to induce HIV-1 replication from latently infected cells in order to render them susceptible to viral cytopathic effects and host immune responses. Whereas HIV treatment has been one of the birthplaces of the concept of combinational therapy, now also spreading to cancer treatment, clinical studies on the activation of latent HIV has remained the domain of single drug treatments. Studies on the regulation of HIV gene expression indicate that alternative pathways and transcription complexes function to regulate the activity of the HIV promoter and might serve as molecular targets for compounds to activate latent HIV. A combined therapy coupling LTR depressors and activators will likely be the most effective in promoting HIV replication while at the same time conferring high specificity for the HIV-1 promoter and avoiding pleiotropic effects at the cellular level. Moreover, the combination of multiple agents will increase likelihood of effectiveness in light of differences in LTR organization among HIV subtypes, and variability in integration sites and at the same time will prevent mutational escape. This review provides an overview of the mechanism that can be targeted to induce HIV activation focusing on potential combinatorial approaches.
Last update: 5 May 2014