Nucleic Acids Research Advance Access originally published online on August 25, 2006
Nucleic Acids Research 2006 34(15):4198-4205; doi:10.1093/nar/gkl398
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Nucleic Acids Research, 2006, Vol. 34, No. 15 4198-4205
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Survey and Summary |
Role of RNA helicases in HIV-1 replication
Molecular Virology Section, Laboratory of Molecular Medicine NIAID, NIH, Bethesda, MD 20892, USA
*To whom correspondence should be addressed. Tel: +1 301 496 6680; Fax: +1 301 480 3686; Email: kj7e{at}nih.gov
Received March 28, 2006. Revised May 10, 2006. Accepted May 11, 2006.
Viruses are replication competent genomes which are relatively gene-poor. Even the largest viruses (i.e. Herpesviruses) encode only slightly >200 open reading frames (ORFs). However, because viruses replicate obligatorily inside cells, and considering that evolution may be driven by a principle of economy of scale, it is reasonable to surmise that many viruses have evolved the ability to co-opt cell-encoded proteins to provide needed surrogate functions. An in silico survey of viral sequence databases reveals that most positive-strand and double-stranded RNA viruses have ORFs for RNA helicases. On the other hand, the genomes of retroviruses are devoid of virally-encoded helicase. Here, we review in brief the notion that the human immunodeficiency virus (HIV-1) has adopted the ability to use one or more cellular RNA helicases for its replicative life cycle.