Multiple viral infections frequently are found in single plants of cultivated and wild hosts in nature, with unpredictable pathological consequences. Synergistic reactions were observed in mixed infections in tomato plants doubly infected with the positive-sense and phloem-limited single-stranded RNA (ssRNA) crinivirus Tomato chlorosis virus (ToCV) and the negative-sense ssRNA tospovirus Tomato spotted wilt virus (TSWV). Synergism in a tomato cultivar susceptible to both viruses resulted in a rapid death of plants. A pronounced enhancement of ToCV accumulation mediated by TSWV co-infection was observed with no evident egress of ToCV from phloem tissues. No consistent alteration of TSWV accumulation was detected. More remarkable was the synergism observed in tomato cultivars which carry the Sw-5 resistance gene, which are resistant to TSWV. Pre-infection with ToCV resulted in susceptibility to TSWV, whereas co-inoculations did not. This suggested that a threshold level or a time lapse is needed for ToCV to interfere or downregulate the defense response in the TSWV-resistant plants.

Tomato-infecting begomoviruses comprise a complex of monopartite and bipartite virus species that cause severe yield and quality losses worldwide. Therefore, the availability of wide spectrum resistance for begomovirus control is desirable. However, limited sources of resistance are available. In this study, three tomato inbred lines with resistance to bipartite begomoviruses of Brazil were tested for resistance to monopartite begomoviruses associated with the tomato yellow leaf curl disease (TYLCD). Stable resistance to Tomato yellow leaf curl virus was observed either by inoculation with Bemisia tabaci or with Agrobacterium tumefaciens using an infectious clone. The resistance resulted in a complete absence of TYLCD symptoms and restricted virus accumulation. Further studies performed with the line '468-1-1-12' indicated that the resistance was also effective against three other virus species associated with TYLCD, indicating wide spectrum resistance of this source. Quantitative genetics analyses suggested that a major recessive locus with epistatic interactions is controlling the resistance to TYLCD in '468-1-1-12', which could facilitate introgression of this trait into elite tomato lines. The resistance was stable under field conditions with high TYLCD pressure. Mild symptoms could be observed in these conditions, and recovery from disease and from virus infection suggested an active host antiviral defense mechanism. The differential reaction of '468-1-1-12' against a number of TYLCD-associated viruses and artificial chimeras between them allowed to identify a region of the virus genome that presumably contains a virus determinant for breaking the resistance to infection observed in '468-1-1-12'.

Tomato chlorosis virus (ToCV) (genus Crinivirus, family Closteroviridae) is an emerging threat to tomato crops worldwide. Although symptoms on fruits are not obvious, yield losses occur through decreased fruit size and number. Control of ToCV epidemics is difficult because the virus is transmitted by several whitefly vector species and its relatively wide host range facilitates establishment in local wild reservoirs. Therefore, breeding for ToCV resistance offers the best control alternative. However, no sources for resistance are available thus far. Here, a screen of tomatoes and wild species relatives was performed in search of ToCV resistance. Two sources of resistance to ToCV were identified in this work, lines '802-11-1' and '821-13-1', each derived by two self-pollinations from ToCV asymptomatic plants of the population 'IAC CN RT' (derived from an interspecific hybrid Solanum lycopersicum x S. peruvianum accession LA0444) and accession LA1028 (S. chmielewskii), respectively. The resistance was expressed by impairing virus accumulation and disease symptom expression, both under natural infection and after challenging with ToCV in controlled inoculations. Genetic control of resistance to ToCV infection in '821-13-1' was conferred by a major locus with mainly additive effects but also partial dominance for higher susceptibility. Also, an additive x dominance epistatic interaction with at least one additional gene was evident.