RNA silencing (RS) is a fundamental plant defence involving small interfering RNA; RS-based resistance is achieved only when viral suppression is avoided. Sweet potato feathery mottle virus (SPFMV), the commonest virus of sweetpotato, induces only transient mild symptoms and associated reversion to healthy, hallmarks of RS defence, provides an alternative to certified virus-free schemes in low-input, developing country farming systems for sweetpotato and other vegetatively-propagated crops, e.g., cassava mosaic-resistant cassava. Sweetpotato virus disease (SPVD), the main disease of sweetpotato in Africa, involves bothSweet potato chlorotic stunt virus (SPCSV) and SPFMV. During co-infection, SPFMV increases in titre, often by several orders of magnitude and apparently in all tissues. SPCSV and SPFMV have already been sequenced. SPCSV has two RNA molecules: two proteins encoded by its RNA 1, p22 and an RNase3 have together been shown to suppress RS, providing a mechanism whereby SPCSV co-infection releases SPFMV from RS-based resistance and causes SPVD. How plants resist viruses through RS will be investigated by studying the known RS system in sweetpotato against SPFMV both in circumstance where resistant sweetpotato resist SPFMV when infecting alone and where it breaks down when co-infecting SPCSV suppresses RS. Diverse germplasm including extreme resistance to SPCSV and SPFMV now identified in CIP’s worldwide sweetpotato collection, SPVD-tolerant African landraces and engineered resistance provide additional research entry points. Sweetpotato is a vital food and nutritional crop in many developing, especially African countries; partners include an African (Uganda) national breeding programme and university. The range and durability of SPFMV RS-based plant resistance, combining ability with other forms of resistance and molecular markers of resistance will be assessed, aiming to achieve rapid deployment of superior resistant varieties and sustainable control