Molecular ecology and emergence of tropical plant viruses.

An appreciation of the risks caused by emergent plant viruses is critical in tropical areas that rely heavily on agriculture for subsistence and rural livelihood. Molecular ecology, within 10 years, has unraveled the factors responsible for the emergence of several of the economically most important tropical plant viruses: Rice yellow mottle virus (RYMV), Cassava mosaic geminiviruses (CMGs), Maize streak virus (MSV), and Banana streak virus (BSV). A large range of mechanisms--most unsuspected until recently--were involved: recombination and synergism between virus species, new vector biotypes, genome integration of the virus, host adaptation, and long-distance dispersal. A complex chain of molecular and ecological events resulted in novel virus-vector-plant-environment interactions that led to virus emergence. It invariably involved a major agricultural change: crop introduction, cultural intensification, germplasm movement, and new genotypes. A current challenge is now to complement the analysis of the causes by an assessment of the risks of emergence. Recent attempts to assess the risks of emergence of virulent virus strains are described.

Methods of surveying the incidence and severity of cassava mosaic disease and whitefly vector populations on cassava in Africa: a review.

Field surveys in many cassava growing areas of Africa have assessed the incidence and severity of cassava mosaic disease (CMD), populations of the whitefly vector (Bemisia tabaci), and the distribution of cassava mosaic begomoviruses (CMBs). The methods employed differ greatly between countries and attempts at standardization were made in recent CMD surveys in East and Central Africa, notably in the systemwide Whitefly IPM Project, which provides a paradigm for future work on CMBs and whiteflies on cassava in Africa and also elsewhere. However, there is a need for greater standardization so as to assess the continued expansion of the current CMD pandemic in eastern Africa. Standardized methods will facilitate the collection of reliable data, which can be used to predict future disease spread, develop appropriate management strategies and compare disease development between seasons and locations. In this review, the methods used and the problems encountered during such surveys are discussed and recommendations made on future procedure.

First Report of a Distinct Begomovirus Infecting Cassava from Zanzibar.

In 1998, cassava plants exhibiting extremely mild mosaic disease symptoms were collected from Uguja Island, Zanzibar. Total DNAs extracted from symptomatic leaves did not produce diagnostic PCR bands using primers specific to known Cassava mosaic viruses (genus Begomovirus, family Geminiviridae) (2). Degenerate primer pair A/B (1), however, produced a 564-nucleotide (nt) band in the common region of DNA-A to the conserved amino acid sequence CEGPCKYG within the coat protein gene for begomoviruses. Virus-specific primers were designed and the begomoviral genome was amplified and cloned to obtain the full-length DNA-A (2,785 nt) (AF422174) and the partial DNA-B (2,403 nt) (AF422175) component comprising the 5' end of the BV1 open reading frame (ORF) to eight (A) of the conserved nanonucleotide TAATATTAC in the common region. Phylogenetic comparisons of DNA-A and -B sequences of the cassava begomivirus showed they were most closely related to East African cassava mosaic virus (EACMV) from Tanzania (Z83256, 83% identity) and Uganda (AF126805, 87% identity). Based on DNA-A and -B components, its closest relatives among African cassava mosaic virus strains were the Nigerian (X17095, 67% identity) and Ugandan (AF126800, 38% identity) isolates respectively. The number and arrangement of the viral ORF was identical to other bipartite begomoviruses from the Old World. Work is in progress to determine whether this begomovirus is a new strain of an existing EACMV or a new species. References: (1) D. Deng et al. Ann. App. Biol. 125:327, 1994. (2) X. Zhou et al. J. Gen. Virol. 78:2101, 1997.

Cassava mosaic virus disease in East Africa: a dynamic disease in a changing environment.

Cassava mosaic disease (CMD), now known to be caused by cassava mosaic geminiviruses (Family Geminiviridae; Genus Begomovirus), was first reported in East Africa in 1894. Epidemics occurred in Madagascar and Uganda in the 1930s and 1940s, and more localised rapid spread of CMD was observed in parts of coastal Tanzania in the 1930s and coastal Kenya in the 1970s. During the 1990s, a major regional pandemic of an unusually severe form of CMD has expanded to affect parts of at least five countries, causing massive economic losses and destabilising food security. Mechanisms responsible for the development and progress of the pandemic have been described, and comparisons of epidemiological data for varieties grown throughout the period under review suggest that the recent pandemic has been characterised by rapid rates of CMD spread hitherto unknown in East Africa. A key factor in the genesis and spread of the pandemic has been the recombination between two distinct cassava mosaic geminiviruses to produce a novel and more virulent hybrid. Although such events may be common, the known history of CMD in East Africa suggests that the frequency with which they become epidemiologically significant is low. A corollary of this is that resistance, developed originally in Tanzania between 1934 and 1960, and utilized and supplemented at the International Institute of Tropical Agriculture, Nigeria, since 1971, is providing effective CMD control in current pandemic-affected areas of East Africa. Consequently, it is concluded that prospects for managing CMD in the 21st century are good, and that the approach adopted should build on the model of collaborative research and implementation that has been established in tackling the current CMD pandemic.