Pathology and Transmission

Infection of O. rhinoceros larvae by Or-lV occurs primarily through the consumption of virus contaminated food, whereas adult insects can become infected when visiting contaminated breeding sites. The virus can also be transmitted by adults during mating, most likely through oral contact with virus from an infected partner. Midgut epithelial cells of both larvae and adults are the primary site of replication and from there the virus spreads to other tissues including the fat body. In larvae, virus replication in the midgut epithelium leads to the appearance of chalky white bodies under the abdominal integument just prior to death of the insect. The abdomen of infected larvae may become turgid and glassy or pearly in appearance. Eventually the fat body disintegrates and the larvae appear translucent.

The disease is commonly fatal in larvae and pupae as well as in adult beetles, however, in adults the infection is often more chronic with infected insects showing no external symptoms of the disease. Virus replication in the adult results in a tumor-like growth of densely packed, virus-filled cells in the midgut which appears swollen and whitish in color. The gut of infected beetles then, becomes filled with virus particles which are eventually defecated. Soon after infection, feeding and egg laying ceases, however, infected adults are capable of flying and mating. Infected beetles usually die within 30 days of infection. During this time these insects can serve as reservoirs and are capable of spreading the virus, via contaminated feces, when visiting breeding sites. Once it was determined that the virus was carried to breeding sites by infected adults, the virus was introduced as a control agent, into pest populations, simply by releasing virus-infected beetles. These releases led to dissemination of the virus in the population and long-term suppression of the rhinoceros beetle on islands in the South Pacific and in Tanzania. Today, a natural equilibrium appears to be established between the level of the virus and the beetle population in these release sites with virus prevalence fluctuating between 30 and 50%.

The agonadal condition caused by Hz-2V results in female moths having enlarged common and lateral oviducts, a deformed bursa copulatrix and malformed or missing ovaries, accessory glands and/or sper-matheca. Affected males have very small testes and are lacking seminal vesicles, vasa deferentia and/or accessory glands. These individuals are sterile and most infected females have a white, 'waxy plug' protruding from the vulva. This plug contains a high concentration of virus particles located inside vesicles which resemble baculovirus occlusion bodies but which lack the dense protein matrix characteristic of occlusion bodies. The replication of Hz-2V appears to be confined to reproductive tissues since the virus is readily observed in the nucleus of cells in these tissues and has not been found in any other tissues of infected animals.

Although most adult moths infected with Hz-2V exhibit agonadal pathology and are sterile, some infected individuals are fertile and can transmit the virus during mating. Both males and females can be asymptomatic carriers of the virus and are capable of transmitting the virus to progeny insects. Larvae and pupae from matings between Hz-2V carriers and uninfected moths appear normal, however, some emerge as sterile, agonadal, adults. Male and female moths injected or fed Hz-2V prior to mating can also transmit the virus to progeny insects. Moreover, it is also possible for the virus to be transmitted on the surface of eggs and by feeding or injecting it into larvae.

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