Origin and Evolution of Defective Interfering RNAs of Tomato Bushy Stunt Virus

Authors

David A. Knorr, University of California, Berkeley
Thomas Jack Morris, University of Nebraska-LincolnFollow

Date of this Version

1991

Citation

Published in Plant Molecular Biology 2. Edited by R.G. Herrmann and B. Larkins. Plenum Press. New York, 1991

Comments

Proceedings of a NATO Advanced Study Institute on Plant Molecular Biology, held May 14-23, 1990, in Elmau, Bavaria, Germany.

Copyright (c) 1991 Plenum Press. Used by permission. (This is the author-furnished version for this camera-ready collection.)

Abstract

Viruses with defective genomes have been identified in association with virtually every major family of viruses and have been widely utilized as tools for investigating virus functions in animal cell culture systems (Perrault, 1981). It is generally thought that defective interfering viruses (DIs) arise through deletion, rearrangement, or recombination of a competent viral genome. DIs tack the ability for independent existence relying on their parental helper viruses to supply factors required for replication, maturation, and/or encapsidation (Huang and Baltimore, 1977). The interference attributed to DIs is thought to result from competition with the helper virus for factors required in trans for replication and/or encapsidation (Schlesinger, 1988). It is these features that have made DIs very useful tools for mapping viral signals required for replication and packaging (e.g. Levis, et aI., 1986). The DIs associated with animal viruses have usually been detected after serial passage of virus at high multiplicities of infection (m.o.i.) in cell cultures. It has also been noted that maintenance in continuous passage results in fluctuations of helper and DI which reflect the relative abilities of each to interfere or support the other (Huang, 1988). DIs have also been detected in natural virus infections and, although there is some debate, may function in vivo to modulate virus diseases and allow more persistent infections (Huang, 1988).

The majority of plant viruses have positive-sense, single-stranded RNA genomes. Additional RNA components capable of modulating symptoms have most commonly been associated with either satellite viruses or satellite RNAs. Satellite viruses differ from satellite RNAs by encoding their own capsid proteins, whereas satellite RNAs are encapsidated by their specific helper virus. Satellite RNAs are relatively common among plant viruses, having been found in association with at least 24 members in six virus groups (Francki, 1985). Unlike DIs, satellite RNAs in general share little sequence similarity with their specific heJper virus . The one exception is the chimeric satellite RNA-C of turnip crinkle virus (Simon, 1988). Satellite viruses and satellite RNAs have been shown to both intensify as well as attenuate symptoms normally expressed by their specific virus helpers (Kaper, and Collmer, 1988, Simon, 1988).

In contrast to the many reports of satellites, few authentic DIs have been identified among plant viruses. These accounts include the presence of DI -Iike particles associated with the negative-stranded plant rhabdoviruses (Adam et al., 1983; Ishmail and Milner, 1988) and the bunyavirus-like tomato spotted wilt virus (Verkleij and Peters, 1983). DI-Iike RNA components have also been reported for wound tumor virus, a plant reovirus (Nuss, 1988). Among the positive, single-stranded RNA plant viruses, authentic DIs have been identified for only two viruses: tomato bushy stunt virus (TBSV) (Hillman et aI., 1987; Morris et al., 1989); and turnip crinkle virus (TCV)(Li et al., 1989).

TBSV and TCV are members of two closely related groups of plant viruses, the tombusviruses and the carmoviruses respectively (see Martelli et al., 1988 and Morris et al., 1988 for reviews). Both viruses are good model systems for studying small RNA virus and DI RNA molecular biology because each has been well-defined biologically and detailed structural studies have been performed on both viruses. In addition, the genome of each virus has been cloned, entirely sequenced, and engineered to produce infectious RNA transcripts in vitro (Carrington et al., 1989; Heaton, et aI., 1989; Hearne, et al., 1990). The reader is referred to these papers for details on the genomic organizations of these two viruses. The features of the TBSV genome organization important in understanding the origins of associated DI RNAs are summarized in Figure 5.

In this paper we will focus on the derivation, molecular characterization, and evolution of TBSV -associated DIs. We will also discuss the possibilities for using plant virus DIs as a general method for controlling virus diseases.