Host Factors in Positive-Strand RNA Virus Genome Replication

• DOI: 10.1128/jvi.77.15.8181-8186.2003
• Publication Date: 2003-07-12T13:13:13Z
• Authors: Paul Ahlquist; Amine O. Noueiry; Wai-Ming Lee; David B. Kushner; Billy T. Dye
• Keywords: Replication; RNA virus

All viruses are gene poor relative to their hosts: even the largest viral genomes only encode hundreds of genes, while those host cells typically tens thousands genes. Thus, most steps in virus infection involve interactions between relatively few different types components and much more complex pools factors. This sea factors represents both essential milieu which must adapt for survival a tremendous, manipulatable resource gene-poor viruses. Accordingly, play important roles infection, identifying such contributions has long been recognized as an frontier. The continuing emergence close integration functions suggests moving beyond separate views holistic view virus-infected cell unified entity that constitutes functional unit infection. One area importance is increasingly emerging replication positive-strand RNA Positive-strand encompass over one-third all genera include numerous pathogens, severe acute respiratory syndrome coronavirus SARS, hepatitis C (HCV), many on U.S. Health Human Services Department Select List potential bioterrorism agents. Host participate most, if not all, including entry, expression, virion assembly, release. Moreover, targeted by modulate expression defenses. review focuses involved positivestrand genome replication. evidence factor involvement come from varied genetic biochemical approaches (15). These include, among others, studies based varying permissiveness some extracts (2, 3, 4, 19); identification proteins interact with genomic RNAs or and, cases, have functionally linked (5, 18, 27, 35, 37, 40); mutational screens model systems, Arabidopsis thaliana (17, 39) yeast Saccharomyces cerevisiae (8, 11, 16, 23, 38). Recent data show assembling complex, selecting recruiting templates, activating synthesis, other steps. Each these virushost may contribute specificity, tissue pathology infections. virus-host interaction also target control optimization improve beneficial uses components. can be divided into number superfamilies defined distinguishable genes features (41). Nevertheless, mechanisms share sufficient similarities make it reasonable discuss class attempt draw general lessons comparing examples superfamilies. As discussed further below, common shared need coordinate use infecting template translation replication, assembly complexes intracellular membranes, production 10- 100-fold excesses positive- negativestrand RNA. A simplified scheme shown Fig. 1. Below we various stages this process, using We regret space limitations do allow us cite work being done exciting area.