Agriculture Reference
In-Depth Information
Attention was given from the outset to the possibility that a new and particularly
damaging form of cassava mosaic virus was spreading to areas where previously
CMD had been relatively benign. However, initial attempts to demonstrate
differences between virus isolates from epidemic and pre-epidemic areas were
unsuccessful. All isolates behaved similarly and had the properties of
African
cassava mosaic virus
(ACMV) in serological tests with monoclonal antibodies
(Harrison
et al.,
1997a). This virus had been detected previously in Uganda and
other parts of Africa west of the Great African Rift Valley, whereas
East African
cassava mosaic virus
(EACMV) occurred in coastal areas to the east and also in
Madagascar (Harrison
et al.,
1995).
Subsequently, PCR primers were used in Uganda to distinguish between isolates
of ACMV that occurred in all districts and those of a distinct virus that occurred in
the many districts that were affected by the epidemic, but not in the few remaining
unaffected areas. The epidemic-associated virus was referred to initially as the
Uganda variant (UgV) (Harrison
et al.,
1997a) or Ugandan cassava virus (UCV)
(Deng
et al.,
1997). It was shown to have the serological properties of ACMV, but
the A component of the DNA genome contains nucleotide sequences of both ACMV
and EACMV. Consequently, UgV/UCV is considered to be a recombinant of the
two viruses.
Additional evidence on the properties of the UgV/UCV recombinant, including
the complete nucleotide sequence of the DNA-B component, was presented by Zhou
et al
. (1997). Moreover, it was shown that plants inoculated with UgV/UCG
developed more severe symptoms than ACMV alone and that dual infection with
both viruses was even more damaging (Harrison
et al.,
1997b). Thus the severe
effects of the epidemic can be explained by the spread of the virulent recombinant
UgV/UCV into areas where previously only ACMV was present and caused
relatively mild symptoms.
In further studies using virus isolates collected in different parts of Uganda
in 1997, the recombinant was re-designated EACMV-UG (Pita
et al.,
2001).
Additional evidence was obtained on the synergism between EACMV-UG and
ACMV and also on the occurrence of mild strains of EACMV-UG (Harrison
et al.,
1997b). There have also been several other studies on the occurrence and
distribution of ACMV and EACMV-UG in different parts of Uganda. These have
shown a decrease in the incidence of ACMV and in the prevalence of dual infection,
together with the increased occurrence of mild strains (Owor
et al.,
2004; Sseruwagi
et al.,
2004). These trends have contributed to the decline in symptom severity that
is a feature of the post-epidemic situation in recent years and one that is also
associated with the adoption of varieties that are resistant to or tolerant of infection
with CMD (Bua
et al.,
2005).
The occurrence and behaviour of the novel recombinant explain many features of
the epidemic in Uganda, but not the big increase in population densities of the
whitefly vector. Moreover, this cannot be attributed to the use or misuse of
insecticides, as recorded with
B. tabaci
on other crops in many parts of Asia and the
Americas (Gerling and Meyer, 1996). This is because insecticides are not widely
used on cotton or other field crops in Uganda and they are not applied at all to
cassava, except by a few farmers who resorted to chemicals in abortive attempts to
