We investigated the genetic pathway in Arabidopsis thaliana targeted during infection by cucumber mosaic virus (CMV) 2b protein, known to suppress non-cell-autonomous transgene silencing and salicylic acid (SA)–mediated virus resistance. We show that 2b expressed from the CMV genome drastically reduced the accumulation of 21-, 22-, and 24-nucleotide classes of viral small interfering RNAs (siRNAs) produced by Dicer-like4 (DCL4), DCL2, and DCL3, respectively. The defect of a CMV 2b–deletion mutant (CMV-Δ2b) in plant infection was efficiently rescued in Arabidopsis mutants producing neither 21- nor 22-nucleotide viral siRNAs. Since genetic analysis further identifies a unique antiviral role for DCL3 upstream of DCL4, our data indicate that inhibition of the accumulation of distinct viral siRNAs plays a key role in 2b suppression of antiviral silencing. Strikingly, disease symptoms caused by CMV-Δ2b in Arabidopsis mutants defective in antiviral silencing were as severe as those caused by CMV, demonstrating an indirect role for the silencing suppressor activity in virus virulence. We found that production of CMV siRNAs without 2b interference depended largely on RNA-dependent RNA polymerase 1 (RDR1) inducible by SA. Given the known role of RDR6-dependent transgene siRNAs in non-cell-autonomous silencing, our results suggest a model in which 2b inhibits the production of RDR1-dependent viral siRNAs that confer SA-dependent virus resistance by directing non-cell-autonomous antiviral silencing.

Plant and animal viruses overcome host antiviral silencing by encoding diverse viral suppressors of RNA silencing (VSRs). Prior to the identification and characterization of their silencing suppression activities mostly in transgene silencing assays, plant VSRs were known to enhance virus accumulation in the inoculated protoplasts, promote cell-to-cell virus movement in the inoculated leaves, facilitate the phloem-dependent long-distance virus spread, and/or intensify disease symptoms in systemically infected tissues. Here we discuss how the various silencing suppression activities of VSRs may facilitate these distinct steps during plant infection and why VSRs may not play a direct role in eliciting disease symptoms by general impairments of host endogenous small RNA pathways. We also highlight many of the key questions still to be addressed on the role of viral suppression of antiviral silencing in plant infection.

SUMMARY: Recent work carried out to characterize recessive mutations which render experimental hosts non‐permissive to viral infection (loss‐of‐susceptibility mutants) seems to be converging with new data on natural recessive resistance in crop species, and also with functional analyses of virus avirulence determinants. Perhaps the most well known examples are the studies that identified the eukaryotic translation initiation factors 4E(iso) (eIF(iso)4E) and 4E(eIF4E) as the host factors required for potyvirus multiplication within experimental and natural hosts, respectively, and the potyviral genome‐linked protein (VPg) as the viral factor that directly interacts with eIF4E to promote potyvirus multiplication. The purpose of this paper is to review the available information on the characterization of loss‐of‐susceptibility mutants in experimental hosts, natural recessive resistances and virus avirulence factors, and also to comment on possible implications for the design of new sources of sustainable virus resistance.

A progressive displacement of tomato yellow leaf curl virus (TYLCV)-Sr by TYLCV-Is was observed in tomato epidemics in southern Spain based on incidence data of both virus species obtained during surveys conducted between 1996 and 1998. Ecological factors that might be involved in such a displacement, such as competition of TYLCV-Sr and TYLCV-Is in tomato, transmission by local biotypes (B and Q) of Bemisia tabaci, and presence in weeds and alternate crops, have been analyzed. No selective advantage is observed for TYLCV-Sr or TYLCV-Is in tomato plants either infected via Agrobacterium tumefaciens or via B. tabaci. However, TYLCV-Is is more efficiently vectored by local biotypes of B. tabaci; and common bean, a bridge crop between tomato crops, is a host for TYLCV-Is but not TYLCV-Sr. Therefore, common bean acts as a reservoir for TYLCV-Is. These two factors are probably responsible for the displacement of TYLCV-Sr by TYLCV-Is as the causative agent of epidemics in tomato in southern Spain.

Field surveys were conducted in the autumn of 1997 in the main tomato (Lycopersicon esculentum)-growing regions of southern Spain following a severe tomato yellow leaf curl epidemic in tomato. Tomato yellow leaf curl virus (TYLCV)-Is was found to have spread to all regions and to coexist with TYLCV-Sr, which has been present since 1992. TYLCV-Is was also shown to be the causal agent of bean leaf crumple, a novel disease that has caused severe economic losses in fresh-market common bean (Phaseolus vulgaris) crops of southern Spain since September 1997. The disease was reproduced by infecting beans with cloned TYLCV-Is obtained from infected tomato plants collected in Almería. This is the first report of bean leaf crumple disease and the first report of a geminivirus in bean from Spain.

SUMMARY: Tomato yellow leaf curl disease (TYLCD) is one of the most devastating viral diseases affecting tomato crops in tropical, subtropical and temperate regions of the world. Here, we focus on the interactions through recombination between the different begomovirus species causing TYLCD, provide an overview of the interactions with the cellular genes involved in viral replication, and highlight recent progress on the relationships between these viruses and their vector, the whitefly Bemisia tabaci . Taxonomy:  The tomato yellow leaf curl virus‐like viruses (TYLCVs) are a complex of begomoviruses (family Geminiviridae , genus Begomovirus ) including 10 accepted species: Tomato yellow leaf curl Axarquia virus (TYLCAxV), Tomato yellow leaf curl China virus (TYLCCNV), Tomato yellow leaf curl Guangdong virus (TYLCGuV), Tomato yellow leaf curl Indonesia virus (TYLCIDV), Tomato yellow leaf curl Kanchanaburi virus (TYLVKaV), Tomato yellow leaf curl Malaga virus (TYLCMalV), Tomato yellow leaf curl Mali virus (TYLCMLV), Tomato yellow leaf curl Sardinia virus ( TYLCSV ), Tomato yellow leaf curl Thailand virus (TYLCTHV) , Tomato yellow leaf curl Vietnam virus (TYLCVNV) and Tomato yellow leaf curl virus (TYLCV). We follow the species demarcation criteria of the International Committee on Taxonomy of Viruses (ICTV), the most important of which is an 89% nucleotide identity threshold between full‐length DNA‐A component nucleotide sequences for begomovirus species. Strains of a species are defined by a 93% nucleotide identity threshold. Host range:  The primary host of TYLCVs is tomato ( Solanum lycopersicum ), but they can also naturally infect other crops [common bean ( Phaseolus vulgaris ), sweet pepper ( Capsicum annuum ), chilli pepper ( C. chinense ) and tobacco ( Nicotiana tabacum )], a number of ornamentals [petunia ( Petunia × hybrida ) and lisianthus ( Eustoma grandiflora )], as well as common weeds ( Solanum nigrum and Datura stramonium ). TYLCVs also infect the experimental host Nicotiana benthamiana . Disease symptoms:  Infected tomato plants are stunted or dwarfed, with leaflets rolled upwards and inwards; young leaves are slightly chlorotic; in recently infected plants, fruits might not be produced or, if produced, are small and unmarketable. In common bean, some TYLCVs produce the bean leaf crumple disease, with thickening, epinasty, crumpling, blade reduction and upward curling of leaves, as well as abnormal shoot proliferation and internode reduction; the very small leaves result in a bushy appearance.