Novel and severe symptoms of chlorosis, rugosity, leaf strapping and dark green islands, designated as sweetpotato severe mosaic disease (SPSMD), were caused by dual infection of Sweet potato mild mottle virus (SPMMV; Ipomovirus) and Sweet potato chlorotic stunt virus (SPCSV; Crinivirus) in three East African sweetpotato cultivars (Tanzania, Dimbuka and New Kawogo). The storage root yield was reduced by ~80%, as compared with healthy plants under screenhouse conditions in Uganda. Plants infected with SPMMV or SPCSV alone showed nonsignificant or 50% yield reduction, respectively. SPCSV reduced resistance to SPMMV in sweetpotato, similar to the situation with resistance to Sweet potato feathery mottle virus (SPFMV; Potyvirus) that breaks down following infection with SPCSV, followed by development of sweet potato virus disease (SPVD). In single virus infections with SPMMV and SPFMV or their coinfection, cvs Tanzania and Dimbuka were initially systemically infected, displayed symptoms and contained readily detectable virus titres, but new leaves were symptomless with very low virus titres, indicating recovery from disease. In contrast, cv. New Kawogo remained symptomless and contained low SPMMV and SPFMV titres following graft inoculation. These moderate and high levels of resistance to SPMMV and SPFMV, respectively, were lost and cultivars succumbed to a severe disease following coinfection with SPCSV. The synergistic interactions increased titres of SPMMV and SPFMV RNA by ~1000-fold as quantified by real-time PCR, whereas SPCSV titres were reduced twofold, indicating an antagonistic interaction. Coinfection with SPMMV and SPFMV caused no detectable changes in virus titres or symptom severity.
- Ipomoea batatas;
- nucleic acid spot hybridization;
- quantitative PCR;