Special Issue "HIV Latency"
Deadline for manuscript submissions: closed (31 July 2014)
Prof. Dr. Fatah Kashanchi
Manuscript Submission Information
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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.