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International Laboratory for Tropical Agricultural Biotechnology (ILTAB)/Donald Danforth Plant Science Center, UMSL/CME-R308, 8001 Natural Bridge Rd, St Louis, MO 63121-4499, USA1
Université de Cocody, Laboratoire de génétique, 22 BP 582 Abidjan 22, Ivory Coast2
Institute of Agronomic Research for Development (IRAD), Ekona PMB 25, Buea South, West Province, Cameroon3
National Agricultural Research Organization, PO Box 7084, Kampala, Uganda4
Author for correspondence: Claude Fauquet. Fax +1 314 516 4582. e-mail iltab{at}danforthcenter.org
The molecular variability of cassava geminiviruses occurring in Uganda was investigated in this study. Infected cassava plants and whiteflies were collected from cassava plantings in different geographical areas of the country and PCR was used for molecular characterization of the viruses. Two complete sequences of DNA-A and -B from African cassava mosaic virus (ACMV), two DNA-A sequences from East African cassava mosaic virus (EACMV), two DNA-B sequences of EACMV and the partial DNA-A nucleotide sequence of a new virus strain isolated in Uganda, EACMV-UG3, are reported here. Analysis of naturally infected cassava plants showed various assortments of DNA-A and DNA-B of the Ugandan viruses, suggesting the occurrence of natural inter- and intraspecies pseudorecombinations and a pattern of cassava mosaic disease (CMD) more complex than previously reported. EACMV-UG2 DNA-A, which contains a recombinant fragment between ACMV and EACMV-UG1 in the coat protein gene that resembles virus from Tanzania, was widespread in the country and always associated with EACMV-UG3 DNA-B, which probably resulted from another natural recombination event. Mixed infections of ACMV-UG and EACMV-UG in cassava and whiteflies were detected in most of the regions where both viruses occurred. These mixed-infected samples always showed extremely severe CMD symptoms, suggesting a synergistic interaction between ACMV-UG and EACMV-UG2. The first demonstration is provided of infectivity of EACMV clones to cassava, proving conclusively that the pseudorecombinant EACMV-UG2 DNA-A+EACMV-UG3 DNA-B is a causal agent of CMD in Uganda.
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