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      Defective Interfering RNAs: Foes of Viruses and Friends of Virologists

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          Abstract

          Defective interfering (DI) RNAs are subviral RNAs produced during multiplication of RNA viruses by the error-prone viral replicase. DI-RNAs are parasitic RNAs that are derived from and associated with the parent virus, taking advantage of viral-coded protein factors for their multiplication. Recent advances in the field of DI RNA biology has led to a greater understanding about generation and evolution of DI-RNAs as well as the mechanism of symptom attenuation. Moreover, DI-RNAs are versatile tools in the hands of virologists and are used as less complex surrogate templates to understand the biology of their helper viruses. The ease of their genetic manipulation has resulted in rapid discoveries on cis-acting RNA replication elements required for replication and recombination. DI-RNAs have been further exploited to discover host factors that modulate Tomato bushy stunt virus replication, as well as viral RNA recombination. This review discusses the current models on generation and evolution of DI-RNAs, the roles of viral and host factors in DI-RNA replication, and the mechanisms of disease attenuation.

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          A viral protein suppresses RNA silencing and binds silencing-generated, 21- to 25-nucleotide double-stranded RNAs.

          Csaba Hornyik, Jozsef Burgyán, Alessandra Lucioli … (2002)
          Posttranscriptional gene silencing (PTGS) processes double-stranded (ds) RNAs into 21-25 nucleotide (nt) RNA fragments that direct ribonucleases to target cognate mRNAs. In higher plants, PTGS also generates mobile signals conferring sequence-specific silencing in distant organs. Since PTGS acts as an antiviral system in plants, successful virus infection requires evasion or suppression of gene silencing. Here we report that the 19 kDa protein (p19) of tombusviruses is a potent silencing suppressor that prevents the spread of mobile silencing signal. In vitro, p19 binds PTGS-generated, 21-25 nt dsRNAs and 21-nt synthetic dsRNAs with 2-nt 3' overhanging end(s), while it barely interacts with single-stranded (ss) RNAs, long dsRNAs or blunt-ended 21-nt dsRNAs. We propose that p19 mediates silencing suppression by sequestering the PTGS-generated 21-25 nt dsRNAs, thus depleting the specificity determinants of PTGS effector complexes. Moreover, the observation that p19-expressing transgenic plants show altered leaf morphology might indicate that the p19-targeted PTGS pathway is also important in the regulation of plant development.
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            New insights into the mechanisms of RNA recombination.

            P D Nagy, A E Simon (1997)
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              Yeast genome-wide screen reveals dissimilar sets of host genes affecting replication of RNA viruses.

              Jeremy Brasher, P. Nagy, Tadas Panavas … (2005)
              Viruses are devastating pathogens of humans, animals, and plants. To further our understanding of how viruses use the resources of infected cells, we systematically tested the yeast single-gene-knockout library for the effect of each host gene on the replication of tomato bushy stunt virus (TBSV), a positive-strand RNA virus of plants. The genome-wide screen identified 96 host genes whose absence either reduced or increased the accumulation of the TBSV replicon. The identified genes are involved in the metabolism of nucleic acids, lipids, proteins, and other compounds and in protein targeting/transport. Comparison with published genome-wide screens reveals that the replication of TBSV and brome mosaic virus (BMV), which belongs to a different supergroup among plus-strand RNA viruses, is affected by vastly different yeast genes. Moreover, a set of yeast genes involved in vacuolar targeting of proteins and vesicle-mediated transport both affected replication of the TBSV replicon and enhanced the cytotoxicity of the Parkinson's disease-related alpha-synuclein when this protein was expressed in yeast. In addition, a set of host genes involved in ubiquitin-dependent protein catabolism affected both TBSV replication and the cytotoxicity of a mutant huntingtin protein, a candidate agent in Huntington's disease. This finding suggests that virus infection and disease-causing proteins might use or alter similar host pathways and may suggest connections between chronic diseases and prior virus infection.
              Article 0 comments Cited 78 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Title: Viruses
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1999-4915
                Publication date Collection: December 2009
                Publication date (Electronic): 10 November 2009
                Volume: 1
                Issue: 3
                Pages: 895-919
                Affiliations
                Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA
                Author notes
                [* ]Authors to whom correspondence should be addressed; E-Mails: kunj@ 123456uky.edu (K.B.P.); pdnagy2@ 123456uky.edu (P.D.N.); Tel: +1 (859) 257-7445/ext 80726; Fax: +1 (859) 323-1961.
                Article
                Publisher ID: viruses-01-00895
                DOI: 10.3390/v1030895
                PMC ID: 3185524
                PubMed ID: 21994575
                SO-VID: 11e33dd9-27b1-4300-b104-de52a6ac4eb4
                Copyright © © 2009 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 20 October 2009
                Date revision received : 9 November 2009
                Date accepted : 9 November 2009
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: recombination,rna virus,rna structure,replication,host factors
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: recombination, rna virus, rna structure, replication, host factors

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