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Cassava is the fourth largest source of calories in the world but is subject to economically important yield losses due to viral diseases, including cassava brown streak disease and cassava mosaic disease. Cassava mosaic disease occurs in sub-Saharan Africa and the Asian subcontinent and is associated with nine begomovirus species, whereas cassava brown streak disease has to date been reported only in sub-Saharan Africa and is caused by two distinct ipomovirus species. We present an overview of key milestones and their significance in the understanding and characterization of these two major diseases as well as their associated viruses and whitefly vector. New biotechnologies offer a wide range of opportunities to reduce virus-associated yield losses in cassava for farmers and can additionally enable the exploitation of this valuable crop for industrial purposes. This review explores established and new technologies for genetic manipulation to achieve desired traits such as virus resistance.

BackgroundCassava mosaic disease is caused by several distinct geminivirus species, including South African cassava mosaic virus-[South Africa:99] (SACMV). To date, there is limited gene regulation information on viral stress responses in cassava, and global transcriptome profiling in SACMV-infected cassava represents an important step towards understanding natural host responses to plant geminiviruses.ResultsA RNA-seq time course (12, 32 and 67 dpi) study, monitoring gene expression in SACMV-challenged susceptible (T200) and tolerant (TME3) cassava landraces, was performed using the Applied Biosystems (ABI) SOLiD next-generation sequencing platform. The multiplexed paired end sequencing run produced a total of 523 MB and 693 MB of paired-end reads for SACMV-infected susceptible and tolerant cDNA libraries, respectively. Of these, approximately 50.7% of the T200 reads and 55.06% of TME3 reads mapped to the cassava reference genome available in phytozome. Using a log2 fold cut-off (p <0.05), comparative analysis between the six normalized cDNA libraries showed that 4181 and 1008 transcripts in total were differentially expressed in T200 and TME3, respectively, across 12, 32 and 67 days post infection, compared to mock-inoculated. The number of responsive transcripts increased dramatically from 12 to 32 dpi in both cultivars, but in contrast, in T200 the levels did not change significantly at 67 dpi, while in TME3 they declined. GOslim functional groups illustrated that differentially expressed genes in T200 and TME3 were overrepresented in the cellular component category for stress-related genes, plasma membrane and nucleus. Alterations in the expression of other interesting genes such as transcription factors, resistance (R) genes, and histone/DNA methylation-associated genes, were observed. KEGG pathway analysis uncovered important altered metabolic pathways, including phenylpropanoid biosynthesis, sucrose and starch metabolism, and plant hormone signalling.ConclusionsMolecular mechanisms for TME3 tolerance are proposed, and differences in patterns and levels of transcriptome profiling between T200 and TME3 with susceptible and tolerant phenotypes, respectively, support the hypothesis that viruses rearrange their molecular interactions in adapting to hosts with different genetic backgrounds.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1006) contains supplementary material, which is available to authorized users.

Cassava brown streak virus disease (CBSD) has been a serious and most damaging disease in cassava crop throughout the East, Central and Southern part of Africa. Several cassava varieties invariably respond to the disease, but the effect of the disease on affected varieties was not known. The current study was conducted to assess the ability of some farmer-preferred CBSD-affected varieties to withstand the disease. Field experiments were conducted at Kibaha Agricultural Research station from 2006 to 2008. The inherent variety characteristics influenced the incidence and severity levels of CBSD in the test plants. Leaf and stem CBSD incidences and severities, root weight and number of whiteflies (vectors) were significantly (P<0.001) related to the individual variety. Varieties Albert, Cheupe, Kibaha and Nachinyaya were seriously affected. The CBSD incidences and severities in these varieties increased with plant age, with highest disease records starting at nine to twelve months after planting. Dual infections of CBSD and CMD were recorded in four (Cheupe, Kibaha, Namikonga and Nachinyaya) of the five test varieties. Namikonga was proven to be resistant to CBSD. The correlation analysis suggested a significantly positive relationship between the perceived disease vector, Bemisia tabaci and the incidence and severities of CBSD and CMD. It was concluded that different varieties responds differently to CBSD and the disease severity increases with plant age.

Plant recovery from viral infection is characterized by initial severe systemic symptoms which progressively decrease, leading to reduced symptoms or symptomless leaves at the apices. A key feature to plant recovery from invading nucleic acids such as viruses is the degree of the host's initial basal immunity response. We review current links between RNA silencing, recovery and tolerance, and present a model in which, in addition to regulation of resistance (R) and other defence-related genes by RNA silencing, viral infections incite perturbations of the host physiological state that trigger reprogramming of host responses to by-pass severe symptom development, leading to partial or complete recovery. Recovery, in particular in perennial hosts, may trigger tolerance or virus accommodation. We discuss evidence suggesting that plant viruses can avoid total clearance but persistently replicate at low levels, thereby modulating the host transcriptome response which minimizes fitness cost and triggers recovery from viral-symptoms. In some cases a susceptible host may fail to recover from initial viral systemic symptoms, yet, accommodates the persistent virus throughout the life span, a phenomenon herein referred to as non-recovery accommodation, which differs from tolerance in that there is no distinct recovery phase, and differs from susceptibility in that the host is not killed. Recent advances in plant recovery from virus-induced symptoms involving host transcriptome reprogramming are discussed.