During November 2004, veinal chlorosis on mature cassava leaves, typical of cassava brown streak disease (CBSD), was observed at Mukono in central Uganda. Five out of 11 cultivars at the site showed CBSD symptoms (incidence range 4 to 64%). In a survey of farmers' fields, CBSD was observed in Wakiso and Mukono districts. Incidence of cassava mosaic disease was also recorded and averaged 60% for landraces (range 16.7 to 100%) and 20% for resistant varieties (range 0 to 65%). Leaf samples of plants with CBSD symptoms produced an amplicon of 222 bp using reverse transcription-polymerase chain reaction with primers that amplify a fragment of the coat protein (CP) gene of Cassava brown streak virus. Sequence comparisons based on the amplified CP gene fragment indicated that the isolates have 77 to 82.9% nucleotide and 43.9 to 56.8% amino acid identity with those from Mozambique and Tanzania. There was 95.9 to 99.5% nucleotide and 85.1 to 90.5% amino acid identity among the Ugandan isolates. These results confirm the re-emergence of CBSD in Uganda after it was first observed in the 1930s in cassava introduced from Tanzania and controlled by eradication. Prior to this report, CBSD was known to be restricted to the coastal lowlands of East Africa.

BackgroundProduction of cassava (Manihot esculenta Crantz), a food security crop in sub-Saharan Africa, is threatened by the spread of cassava brown streak disease (CBSD) which manifests in part as a corky necrosis in the storage root. It is caused by either of two virus species, Cassava brown streak virus (CBSV) and Ugandan cassava brown streak virus (UCBSV), resulting in up to 100% yield loss in susceptible varieties.MethodsThis study characterized the response of 11 cassava varieties according to CBSD symptom expression and relative CBSV and UCBSV load in a field trial in Uganda. Relative viral load was measured using quantitative RT-PCR using COX as an internal housekeeping gene.ResultsA complex situation was revealed with indications of different resistance mechanisms that restrict virus accumulation and symptom expression. Four response categories were defined. Symptom expression was not always positively correlated with virus load. Substantially different levels of the virus species were found in many genotypes suggesting either resistance to one virus species or the other, or some form of interaction, antagonism or competition between virus species.ConclusionsA substantial amount of research still needs to be undertaken to fully understand the mechanism and genetic bases of resistance. This information will be useful in informing breeding strategies and restricting virus spread.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-014-0216-x) contains supplementary material, which is available to authorized users.

Cassava (Manihot esculenta Crantz) production is currently under threat from cassava brown streak disease (CBSD), a disease that is among the seven most serious obstacles to world’s food security. Three issues are of significance for CBSD. Firstly, the virus associated with CBSD, has co-evolved with cassava outside its center of origin for at least 90 years. Secondly, that for the last 74 years, CBSD was only limited to the low lands. Thirdly, that most research has largely focused on CBSD epidemiology and virus diversity. Accordingly, this paper focuses on CBSD genetics and/or breeding and hence, presents empirical data generated in the past 11 years of cassava breeding in Uganda. Specifically, this paper provides: 1) empirical data on CBSD resistance screening efforts to identify sources of resistance and/or tolerance; 2) an update on CBSD resistance population development comprising of full-sibs, half-sibs and S1 families and their respective field performances; and 3) insights into chromosomal regions and genes involved in CBSD resistance based on genome wide association analysis. It is expected that this information will provide a foundation for harmonizing on-going CBSD breeding efforts and consequently, inform the future breeding interventions aimed at combating CBSD.

Cassava brown streak disease (CBSD) has occurred in the Indian Ocean coastal lowlands and some areas of Malawi in East Africa for decades, and makes the storage roots of cassava unsuitable for consumption. CBSD is associated with Cassava brown streak virus (CBSV) and the recently described Ugandan cassava brown streak virus (UCBSV) [picorna-like (+)ssRNA viruses; genus Ipomovirus; family Potyviridae]. This study reports the first comprehensive analysis on how evolution is shaping the populations of CBSV and UCBSV. The complete genomes of CBSV and UCBSV (four and eight isolates, respectively) were 69.0-70.3 and 73.6-74.4 % identical at the nucleotide and polyprotein amino acid sequence levels, respectively. They contained predictable sites of homologous recombination, mostly in the 39-proximal part (NIbHAM1h-CP-39-UTR) of the genome, but no evidence of recombination between the two viruses was found. The CP-encoding sequences of 22 and 45 isolates of CBSV and UCBSV analysed, respectively, were mainly under purifying selection; however, several sites in the central part of CBSV CP were subjected to positive selection. HAM1h (putative nucleoside triphosphate pyrophosphatase) was the least similar protein between CBSV and UCBSV (aa identity approx. 55 %). Both termini of HAM1h contained sites under positive selection in UCBSV. The data imply an on-going but somewhat different evolution of CBSV and UCBSV, which is congruent with the recent widespread outbreak of UCBSV in cassava crops in the highland areas (.1000 m above sea level) of East Africa where CBSD has not caused significant problems in the past.

Cassava (Manihot esculenta Crantz) is an important security crop that faces severe yield loses due to cassava brown streak disease (CBSD). Motivated by the slow progress of conventional breeding, genetic improvement of cassava is undergoing rapid change due to the implementation of quantitative trait loci mapping, Genome-wide association mapping (GWAS), and genomic selection (GS). In this study, two breeding panels were genotyped for SNP markers using genotyping by sequencing and phenotyped for foliar and CBSD root symptoms at five locations in Uganda. Our GWAS study found two regions associated to CBSD, one on chromosome 4 which co-localizes with a Manihot glaziovii introgression segment and one on chromosome 11, which contains a cluster of nucleotide-binding site-leucine-rich repeat (NBS-LRR) genes. We evaluated the potential of GS to improve CBSD resistance by assessing the accuracy of seven prediction models. Predictive accuracy values varied between CBSD foliar severity traits at 3 months after planting (MAP) (0.27–0.32), 6 MAP (0.40–0.42) and root severity (0.31–0.42). For all traits, Random Forest and reproducing kernel Hilbert spaces regression showed the highest predictive accuracies. Our results provide an insight into the genetics of CBSD resistance to guide CBSD marker-assisted breeding and highlight the potential of GS to improve cassava breeding.