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  • Author or Editor: Douglas Miano x
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Sweetpotato is an important staple food crop in Sub-Saharan Africa, with production being concentrated in East Africa, particularly around Lake Victoria. Productivity of the crop is greatly constrained by viral diseases. Four main viruses have consistently been detected from various surveys done in the region viz., sweetpotato feathery mottle virus (SPFMV), sweetpotato chlorotic stunt virus (SPCSV), sweetpotato mild mottle virus (Sp.m.MV), and sweetpotato chlorotic fleck virus (SPCFV). The most severe symptoms have been caused by co-infection with SPCSV and SPFMV, resulting in the synergistic sweetpotato virus disease (SPVD). Some local sweetpotato genotypes have been reported to recover from, or have localized distribution of SPVD, suggesting that the disease is not fully systemic. This has led to the suggestion that uninfected cuttings may be obtained from previously infected plants. Experiments were set to determine the possibility of obtaining cuttings long enough for propagation that are free from virus infection. This would form a basis for recommending to the local small-holder farmers of a way to reduce losses due to the disease. Field-grown sweetpotato vines were cut into three pieces (15, 15–30, and >30 cm from the apex) and tested for SPCSV and SPFMV. Nine genotypes were selected from a group of 21 local clones and used for this study. The two viruses were equally present in all the three sections of infected vines, indicating that it is not easy to obtain a virus-free cutting for field propagation from an infected vine. Virus assays in the past has mainly been limited to the use of serological methods. Use of PCR resulted in detection of begomoviruses infecting sweetpotatoes for the first time in the region.

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Sweet potato virus disease (SPVD) is one of the most devastating diseases affecting sweetpotato (Ipomoea batatas), an important food crop in developing countries. SPVD develops when sweetpotato plants are dually infected with sweet potato feathery mottle virus (SPFMV) and sweet potato chlorotic stunt virus (SPCSV). To better understand the synergistic interaction between these viruses, global gene expression was previously studied in the susceptible cultivar Beauregard. In the current study, global gene expression between SPVD-affected plants and virus-tested control plants (VT) were compared in ‘Beauregard’ (Bx) and resistant ‘NASPOT 1’ (Nas) sweetpotato cultivars at 5, 9, 13, and 17 days post inoculation (DPI). Titer levels of SPFMV and SPCSV were significantly lower in inoculated resistant plants (Nas_SPVD) than in susceptible plants (Bx_SPVD) at most of the time points. Chloroplast genes and cell expansion-related genes (including xyloglucan endotransglucosylase/hydrolases) were suppressed in Bx_SPVD, while stress-related genes were induced. This trend was not observed in resistant NAS_SPVD. Genes related to protein synthesis (e.g., ribosomal proteins and elongation factor genes) were induced in resistant NAS_SPVD at 5 DPI before returning to levels comparable with NAS_VT plants. At this time (5 DPI), individual viruses could not be detected in NAS_SPVD samples, and no symptoms were observed. Induction of protein synthesis-related genes is common in susceptible plants after virus infection and is generally in proportion to virus accumulation. Our results show that induction of protein synthesis genes also occurs early in the infection process in resistant plants, while virus titers were below the level of detection, suggesting that virus accumulation is not required for induction.

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