期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 11, 期 -, 页码 89-112出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/1782
关键词
virus; immune deficiency; HIV; AIDS; viral expression; Rev; RRE; Tat; TAR); viral packaging; p55Gag; matrix; nucleocapsid; viral entry; gp120; review
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 ( p55(Gag), 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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