To study the cause of the current epidemic of severe mosaic in Ugandan cassava, PCR analysis was used to detect and identify African cassava mosaic virus (ACMV), East African cassava mosaic virus (EACMV) and the recently reported recombinant geminivirus (UgV), which is derived from ACMV and EACMV, in leaf extracts from cassava plants grown from cuttings in the glasshouse at Dundee. The cuttings were collected from plants showing symptoms of different severities and growing at different sites in Uganda inside, at the periphery of, and outside, the area affected by the epidemic. ACMV occurred throughout the nine districts sampled but UgV was detected only in the area affected by the epidemic. EACMV was not found in Uganda. Most plants containing ACMV alone expressed mild or moderate mosaic, whereas very severe mosaic developed in most plants containing UgV plus ACMV and a few of those containing UgV only. Very severe mosaic in cassava from southern Sudan was likewise associated with co-infection by UgV and ACMV. The very severe disease was reproduced by graft-inoculating geminivirus-free cassava with UgV plus ACMV; plants inoculated with either UgV or ACMV developed severe or moderate symptoms, respectively. Unlike ACMV, Malawian EACMV did not enhance the severity of symptoms induced by UgV. However, a very severely affected plant from Ukerewe Island, Tanzania, contained ACMV and EACMV but not UgV. UgV attained a much greater concentration in cassava than did ACMV but the opposite occurred in Nicotiana benthamiuna. In neither host was total virus antigen concentration affected by co-infection.Factors affecting the genesis, selection and spread of UgV are discussed. The evidence indicates that UgV is probably of relatively recent origin, that such variants do not appear often, and that the current epidemic has resulted from the rapid spread of UgV to infect plants and to invade regions in which ACMV already occurred. The novel type of virus complex so produced, consisting of an interspecific recombinant virus (UgV) and one of its parents (ACMV), typically has even more severe effects than UgV alone. 0 1997 Association of Applied Biologists 438 B D HARRISON ET AL.

Begomoviruses have circular single-stranded DNA genomes, cause many diseases of dicotyledons in areas with warm climates and are transmitted by whiteflies of the Bemisia tabaci complex. Their genomic and antigenic variation represents geography-related lineages that have little relation to host range. Genomic variation resulting from mutation is amplified by acquisition of extra DNA components, pseudo-recombination and recombination, both intraspecific and interspecific. Recombination, especially interspecific recombination, seems the key mechanism for generating novel virus forms, for enhancing biological fitness of pseudo-recombinants derived from closely related species and for maintaining the flow of genetic material among different geminiviruses occurring in the same geographical region. Recent begomovirus epidemics reflect favorable conjunctions of plant, vector, and viral (e.g. emergence of a novel recombinant virus) factors. Such epidemics typically result in co-infection of plants with different begomoviruses, leading to the appearance of further variants, especially recombinants. In their patterns of variation and evolution, begomoviruses differ greatly from plant viruses with RNA genomes.

SUMMARYIn hybridization experiments, using complementary DNA (cDNA) copies of the two genome parts of tomato black ring virus (TBRV RNA-I and RNA-2), no sequence homology between the two RNA species was detected.When tobacco mesophyll protoplasts were inoculated with purified middle component particles, which contain only RNA-2, no replication of TBRV RNA could be detected. However, when they were inoculated with purified bottom component particles, which contain only RNA-L extracts made 24 or 48 h later contained RNA that had the same mobility as RNA-~ in polyacrylamide-agarose gels, and that hybridized to cDNA copies of RNA-I. Thus RNA-1 can replicate in protoplasts that do not contain RNA-2. Moreover, this RNA-1 was capable, when mixed with nucleoprotein particles containing RNA-2, of inducing the formation of local lesions in Chenopodium amaranticolor leaves, and therefore was intact and attached to the genome-linked protein. The genome-linked protein of nepoviruses is probably virus-coded, and its production in protoplasts inoculated with bottom component particles therefore suggests that RNA-t contains the gene for this protein.

Patterns of variation are examined in four groups of plant viruses, with special reference to their particle proteins and to changes in vector transmissibility and specificity. In the nepoviruses and potyviruses, non-circulative transmission, by nematodes and aphids respectively, seems dependent on structural features on the surface of the virus particles. The N-terminal part of the particle protein may play the key role in potyviruses. Similarly in the luteoviruses, and possibly in the geminiviruses, specificity of circulative transmission by aphids, whiteflies and leafhoppers is linked to the antigenic specificity of the virus particles. Among naturally occurring isolates of the same virus, variation seems often to be discontinuous, and is predominantly of two sorts. Minor variations, characterized by loss of an epitope or substitutions of a few amino acids, can be associated with loss of transmissibility in luteoviruses and potyviruses, or have no effect. Major variations are associated with differences in vector specificity and seem likely to involve radical genetic changes that have evolved over long periods. The adaptation of virus particle proteins for transmission by vectors probably results in conservation of the genes that encode them, and in greater conservation of some parts of these genes than of others.

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