IMR Press / FBL / Volume 11 / Issue 1 / DOI: 10.2741/1782

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
HIV-1 inactivation by nucleic acid aptamers
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1 Department of Biology, Indiana University, Bloomington, IN 47405, USA
2 Departments of Chemistry, Indiana University, Bloomington, IN 47405
3 Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212
Academic Editor:Vinayaka Prasad
Front. Biosci. (Landmark Ed) 2006, 11(1), 89–112; https://doi.org/10.2741/1782
Published: 1 January 2006
(This article belongs to the Special Issue RNA therapeutics for AIDS)
Abstract

Although developments in small-molecule therapeutics for HIV-1 have been dramatic in recent years, the rapid selection of drug-resistant viral strains and the adverse side effects associated with long-term exposure to current treatments propel continued exploration of alternative anti-HIV-1 agents. Non-coding nucleic acids have emerged as potent inhibitors that dramatically suppress viral function both in vitro and in cell culture. In particular, RNA and DNA aptamers inhibit HIV-1 function by directly interfering with essential proteins at critical stages in the viral replication cycle (Figure 1). Their antiviral efficacy is expected to be a function, in part, of the biochemical properties of the aptamer-target interaction. Accordingly, we present an overview of biochemical and cell culture analyses of the expanding list of aptamers targeting HIV-1. Our discussion focuses on the inhibition of viral enzymes (reverse transcription, proteolytic processing, and chromosomal integration), viral expression (Rev/RRE and Tat/TAR), viral packaging (p55Gag, matrix and nucleocapsid), and viral entry (gp120) (Table 1). Additional nucleic acid-based strategies for inactivation of HIV-1 function (including RNAi, antisense, and ribozymes) have also demonstrated their utility. These approaches are reviewed in other chapters of this volume and elsewhere (1-5).

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