There have been a number of reports of DNV diseases of economically important insects in Japan and the Peoples' Republic of China. A disease of the silkworm B. mori in the vicinity of Ina City, Japan, in 1968 has led to the discovery of B/wDNV. At least two other isolates of DNV from diseased silkworms were later discovered in Japan and in China. Epizootic spread of DNV was observed in Japan in silkworm sericulture farms and in mulberry pyralids in mulberry plantations. The virus isolated from the mulberry pyralid was serologically indistinguishable from B/mDNV-1 and was infectious to BwDNV-l-susceptible silkworm strains, suggesting that they are either identical or have a common origin. DNV antigen was detected in the dust collected from several silkworm-rearing farms in Japan, in which BwDNV-resistant silkworm strains are being used. These findings are interpreted to suggest that enzootic distribution of BmDNV is widespread, and probably demonstrate that epizootics are prevented by the use of nonsusceptible silkworm strains.
Some evidence suggests that immunity to infection may play a role in the spread of disease by DNVs. Primarily, extracts from uninfected Galleria larvae were found to contain substances with affinity to, or associated with GwiDNV. There is no evidence for acquired immunity.
Although some DNVs inflict economical damage, others are considered as potential biological control agents. Some success has been reported using the virus as an insecticide. In Columbia, extracts of DNV-infected larvae were used to control the disease of palm trees caused by Sibine fusca, and in the Ivory Coast DNV has been highly successful in the eradication of Casphalia extranea, a pest of oil palm and coconut trees. The advantages of DNV as pest control agents are the high resistance of the virions to environmental conditions such as heat and organic solvents and their high infectivity ratios to susceptible insects. The major disadvantage is that the extreme sensitivity of these ssDNA-containing, nonenveloped virions to UV radiation imposes limitations on their use as insecticides.
Densoviruses differ in their pathology and tissue specificity; some (e.g. Gm, /cDNVs) can cause an extensive viremia in most or all tissues, whereas the replication of others, such as Sibine DNV, is restricted primarily to the midgut. BmDNV multiplies only in the nuclei of the columnar cells of the midgut epithelium columnar cells.
DNV-caused disease is lethal, and is characterized by the accumulation of DNV particles in the nuclei of infected cells. The nuclei degenerate gradually and vacuoles and inclusion bodies appear in the cytoplasm. In the nucleus, the virus forms multilayer crystalline-like structures which occupy the majority of the nucleoplasm volume. The infected larvae become anorexic, sluggish and flaccid, and are progressively paralyzed. Death occurs within 5—10 days, depending on the larval stage, multiplicity of infection and environmental conditions.
DNV histopathology can assume many forms. In AeDNV infected Aedes aegypti larvae, the nuclei of the infected cells (hypodermis, imaginal disk, endocrine glands, trachea, hypodermis, etc.) become double in size of those of normal cells and intranuclear structures are disrupted. In G/wDNV infection the nuclei of the midgut cells become hypertrophied and eosinophilic, and dense bodies accumulate in the nucleoplasm. S. fusca DNV produces distinct pathological changes: the digestive tracts of the infected larvae become thickened, opaque and whitish.
DNV infections of last instar larvae often result in inhibition of pupation. Infection at lower concentrations results in partial metamorphosis, but larval tissues in the pupae are affected. Silk production and cocoon spin are also inhibited.
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