Interfering Replicons

During natural virus infections replicons may accumulate that are derived from the master virus but have a smaller size (105) or are predominantly unrelated to the helper virus (satellites) (68). Moreover, some replicons appeared to be recombination products of a helper virus nucleic acid and unrelated sequences (106). These additional replicons might enhance the effect of the virus, ameliorate the symptoms, or behave neutrally (68). When they interfere with virus multiplication or symptom development, they are called defective interfering (DI) nucleic acids.

1. Defective Interfering (DI) Nucleic Acids

DI nucleic acids have been observed for RNA- and DNA-containing viruses (105,107). DI-DNA molecules of geminiviruses have attracted special interest (Fig. 2). Geminiviruses encapsidate single-stranded circular DNA and replicate in nuclei. Over the past three decades they raised worldwide devastating epidemics, predominantly in tropical and subtropical countries (108,109) but also in the United States (beet curly top virus, BCTV) (110) and around the Mediterranean sea (tomato yellow leaf curl virus, TYLCV) (111). Their genomes consist of either one component (genera Mastre-, Curto-, and Topocuvirus) or two components (most of the genus Begomo-virus), which are called DNA A and DNA B (112). DI-DNA has been investigated in more detail for BCTV, with a set of half and smaller size DNA circles from a single genomic component (113) (Fig. 2), and for African cassava mosaic begomovirus, which accumulates smaller molecules derived from the DNA B component (114,115). All these DI molecules harbor the origin of replication and parts of predominantly the left halves of the genomic components. They usually do not contain intact open reading frames with the exception of BCTV-DI, possessing the small ORF C4 influencing symptom expression (116).

Integrating tandem copies of DI-DNA into plant chromosomes does not disturb the development of plants, and DI-DNA is not replicated because

Figure 2 Defective-interfering (Dl) DNA of beet curly top geminivirus (BCTV) to protect plants from virus infection. Open reading frames are named according to their complementary (C) or viral (V) orientation. IR assigns the intergenic region harboring viral promoters and the origin of replication. Bit-mers (x1.5) were integrated into plant chromosomes, which are transrepli-cated upon infection with the cognate virus (BCTV).

Figure 2 Defective-interfering (Dl) DNA of beet curly top geminivirus (BCTV) to protect plants from virus infection. Open reading frames are named according to their complementary (C) or viral (V) orientation. IR assigns the intergenic region harboring viral promoters and the origin of replication. Bit-mers (x1.5) were integrated into plant chromosomes, which are transrepli-cated upon infection with the cognate virus (BCTV).

the viral replication initiator protein (AC1 or CI) is lacking. Upon challenge by the cognate virus, DI-DNA replicates and symptoms are ameliorated, leading to a recovery after longer time periods of infection (114,115,117). During this process, DI-DNA accumulates and full-length viral DNA is reduced compared with infection of control plants. It has been suggested that down-regulation of viral multiplication is caused by the competition of DI-DNA with viral DNA for replication complexes, but it is not completely excluded that intact proteins (C4), defective proteins (AAC1, ABC1) as dominant-negative effectors, or RNA-mediated processes participate in the protection (105). In this context it is interesting to note that smaller DI-DNA may replicate to even higher levels, but such an increase did not lead to enhanced inhibition (118). DI-DNA is packed into half-size particles (119) and the amount of DI molecules is elevated after serial passages to further plants, rendering this strategy especially useful for field applications.

A limitation results from the necessity to recognize a specific origin of replication by the compatible replication-associated (Rep) protein of the cognate virus to induce DI-DNA multiplication. Therefore, DI-DNA can act only against closely related viruses that are able to transreplicate each other.

2. Satellites

Satellites are small, a few hundred nucleotides in size, RNA (satRNA) or DNA (satDNA) molecules that are transreplicated by a helper virus (67,68). Some of them, encoding their own coat protein for packaging their RNA, are called satellite viruses. The other satellites might also contain small open reading frames (ORFs) of unknown function.

Satellites modulate symptom expression of their helper virus, either increasing or decreasing severity. Their particular effects are governed by the triangular interrelationship between virus strain, satellite, and host genotype. Expression of putative proteins from ORFs of satRNAs has been prevented by site-directed mutagenesis without abolishing symptom modulation (65). Therefore, it is believed that the secondary structure determines the effect rather than the coding capacity of the RNA.

It was shown in model plants that satRNA expressed from transgenes can confer some protection against the helper virus effects (70,71). For field application this approach was frequently questioned, especially because of the variability of possible effects upon coinfection with other viruses or because satRNA might be transferred to other nontarget hosts (65,68,69). Nevertheless, this strategy using either classical coinoculation techniques or transgenic means has been successfully applied in Asia (72-75), resulting in a considerable reduction of yield losses.

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