|Lietze, Verena-Ulrike - UNIVERSITY OF FLORIDA|
|Blackburn, Patrick - UNIVERSITY OF FLORIDA|
|Boucias, Drion - UNIVERSITY OF FLORIDA|
Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 1, 2007
Publication Date: November 1, 2007
Citation: Lietze, V., Geden, C.J., Blackburn, P., Boucias, D.G. 2007. Effects of salivary gland hyperplasia virus on reproductive behavior of the house fly, Musca domestica. Applied and Environmental Microbiology. 73:6811-6818. Interpretive Summary: House flies are important pests associated with animals and humans and transmit a wide array of disease organisms. Efforts to manage flies have traditionally relied on chemical insecticides, but flies have become resistant to most insecticides and there is increasing public demand to reduce pesticide use around animals that are used in the production of meat, milk and eggs. Most biological control research on flies has concentrated on targeting fly pupae with parasitic wasps. In contrast, efforts to manage adult flies has been restricted to pathogenic fungi, with mixed results. In this paper, scientists at the University of Florida and USDA-ARS’s Center for Medical, Agricultural and Veterinary Entomology (Gainesville, FL) report on a novel viral disease of adult flies. The virus is spread when infected flies regurgitate on food that is then fed upon by healthy flies. Once they are infected, female flies are unable to metabolize protein meals properly and fail to develop eggs. Infected female and male flies are also less successful in their mating behavior. Because infected flies neither mate readily nor lay eggs, the virus could serve as an important natural control agent that could be manipulated to limit fly population growth early in the fly season.
Technical Abstract: Pathological studies demonstrated that the salivary gland hyperplasia virus of house flies (MdSGHV) shuts down reproduction in infected females. The mechanism that underlies the disruption of reproduction functioned onat several levels. Females infected at the pre-vitellogenic stage did not produce eggs, reflecting a block in the gonadotropic cycle. SDS-PAGE and western blot analysis on hemolymph samples demonstrated that MdSGHV infection reduced levels of both the female specific hexamerin and egg yolk proteins. Furthermore, qRT-PCR data demonstrated that infection blocked hexamerin and the yolk protein gene transcription. If females were allowed to develop eggs prior to infection (post-vitellogenic stage), the outcomes of mating attempts depended upon when mating was allowed to take place. If the egg-containing, virus-infected females were mated within 24 h of infection, they copulated and deposited a single batch of fertilized eggs. However, if mating was delayed for a longer period, then these egg-containing females refused to copulate with healthy males. Both of these results suggested that a virus-induced signal influenced the CNS, shutting down female receptivity and egg production. All experiments demonstrated that MdSGHV-infected males did not display azoospermia and were fertile. Both the healthy females mated with infected males and the resulting F1 progeny were free of SGH symptoms, which suggestsing that this virus is not sexually or vertically transmitted.