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32 - Lost in translation: regulation of HIV-1 by microRNAs and a key enzyme of RNA-directed RNA polymerase

from V - MicroRNAs in disease biology

Published online by Cambridge University Press:  22 August 2009

By
Yoichi Robertus Fujii
Edited by
Krishnarao Appasani
Foreword by
Sidney Altman  and
Victor R. Ambros
Yoichi Robertus Fujii
Affiliation:
Molecular Biology and Retroviral Genetics Group Division of Nutritional Sciences Graduate School of Pharmaceutical Sciences Nagoya City University Nagoya 467-8603 Japan
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Summary

The annual labor of every nation is the fund which originally supplies it with all the necessaries and conveniences of life which it annually consumes, and which consist always either in the immediate produce of that labor, or in what is purchased with that produce from other nations.

Adam Smith

Introduction

The human immunodeficiency virus type 1 (HIV-1) gene, nef, is located at the 3′ end of the viral genome and partially overlaps the 3′-long terminal repeat (LTR). The nef gene is expressed during HIV infection and often accounts for up to 80% of HIV-1-specific RNA transcripts during the early stages of viral replication (Robert-Guroff et al., 1990). Because HIV-1 LTR activity is down-regulated just a few hours after induction by Tat, this may contribute to viral latency (Drysdale and Pavlakis, 1991). However, the mechanism of this down-regulation of Tat transactivation as well as accumulation of nef RNAs is not completely clear. MicroRNAs (miRNAs) are 21–25 nucleotides (nt) long and directed selectively to targeting sequences of mRNAs to trigger either translational repression or RNA cleavage through RNA interference (RNAi) (Zeng et al., 2003; Yekta et al., 2004). However, RNAi had not been found in mammals by functional assays, as observed naturally in plants, fungi, insects or nematodes (Fire et al., 1998; Tuschl et al., 1999; Ketting et al., 1999; Tabara et al., 1999; Aravin et al., 2001; Baulcombe, 2001; Sijen and Plasterk, 2003).

Type
Chapter
Information
MicroRNAs
From Basic Science to Disease Biology
 , pp. 427 - 442
Publisher: Cambridge University Press
Print publication year: 2007

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