Open access publications in the SLU publication database

Abstract

The studies presented in this thesis contribute to improved understanding of genetic variability and interactions of the most prevalent sweetpotato infecting viruses in Uganda. Sweet potato feathery mottle virus (SPFMV; genus Potyvirus), Sweet potato mild mottle virus (SPMMV; genus Ipomovirus), Sweet potato chlorotic stunt virus (SPCSV; genus Crinivirus) and Sweet potato chlorotic fleck virus (SPCFV; genus Carlavirus) were serologically detected, and the positive results were confirmed by RT-PCR and sequence analysis. Molecular phylogenetic studies revealed high genetic variability in SPMMV and SPFMV whereas SPCSV isolates from East Africa seem less variable. At a molecular level, strains are now more recognised in SPFMV and SPMMV. Co-infections of SPCSV with SPFMV and/or SPMMV were associated with persistent and more severe symptoms than infections with each of the viruses alone, and were responsible for over 90% of the field diseased plants. Novel and severe symptoms including chlorosis, rugosity, leaf strapping and dark green islands caused by the dual infection of SPMMV and SPCSV were observed. These symptoms could be differentiated from those caused by dual infection of SPFMV and SPCSV that is associated specifically with the sweetpotato virus disease (SPVD), characterised by often severe stunting of the plant, distortion and either chlorotic mottle or vein clearing of the leaves. These observations show SPCSV, SPFMV and SPMMV to be the most important viruses of sweetpotato in Uganda. The name “sweetpotato severe mosaic disease” (SPSMD) is proposed to describe the disease caused by the dual infection of SPMMV and SPCSV. A comparative analysis of the interaction between the phloem-limited SPCSV and either SPFMV or SPMMV indicated more severe disease symptoms and much higher tuber yield reduction as compared to singly infected plants. Immunohistochemical localisation of SPMMV in sweetpotato plants suggest that it could be exploiting niches (mesophyll, companion and epidermal cells) similar to those of SPFMV. SPMMV and SPFMV RNA accumulation greatly increased by over 32 and 64 fold, respectively, in mixed infection with SPCSV. However, accumulation of SPCSV in mixed infection with SPMMV or SPFMV was reduced by 2-4 fold, indicating an antagonistic interaction. Neutral (non-detectable) interactions were observed between SPFMV and SPMMV. The synergistic, antagonistic and neutral interactions were observed in plants of the three sweetpotato cultivars, suggesting that they may represent typical interactions of three viruses. These findings further show the importance of SPCSV in elevating virulence of SPFMV and SPMMV, by suppressing the otherwise high levels of host resistance to single infections in East African sweetpotato cultivars. Efforts to particularly control SPCSV (e.g. through RNA-mediated resistance, use of clean planting materials) and improved knowledge on various aspects of the ecology of sweetpotato viruses in Uganda seem to be the next necessary steps towards better management strategies for sweetpotato viral diseases.