Pathological studies demonstrated that the salivary gland hypertrophy virus of houseflies (MdSGHV) shuts down reproduction in infected females. The mechanism that underlay the disruption of reproduction functioned on several levels. Females infected at the previtellogenic stage did not produce eggs, reflecting a block in the gonadotropic cycle. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis of hemolymph samples demonstrated that MdSGHV infection reduced the levels of both the female-specific hexamerin and egg yolk proteins. Furthermore, reverse transcriptase quantitative real-time PCR data demonstrated that infection blocked hexamerin and yolk protein gene transcription. When females were allowed to develop eggs prior to infection (postvitellogenic stage), the outcome of mating attempts depended upon when mating took place. If 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, the egg-containing females refused to copulate with healthy males. Both of these results suggested that a virusinduced signal influenced the central nervous system, shutting down female receptivity and egg production. All experiments demonstrated that MdSGHV-infected males did not display azoospermia and were fertile. Both healthy females mated with infected males, and the resulting F1 progeny were free of salivary gland hypertrophy symptoms, which suggests that the virus is not sexually or vertically transmitted.In the early 1990s, an insect virus was detected and isolated from hypertrophied salivary glands of male and female houseflies, Musca domestica L., in Florida. The virus was described initially as a nonoccluded, enveloped, rod-shaped, doublestranded DNA virus (7). Feeding bioassays demonstrated that the virus could be transmitted per os to healthy adult houseflies and that infection with the virus was responsible for the salivary gland hypertrophy (SGH) symptoms. In these experiments, 95% of the female houseflies with symptoms of SGH showed no sign of ovarian development (7). A similar virus causing symptoms of SGH has been reported in the narcissus bulb fly, Merodon equestris (Fabricius) (3), and in various species of tsetse flies, Glossina spp. (3, 11). Comparisons of the different virus-host fly systems have demonstrated that the different viruses have several morphological and pathological properties in common (3,7,8,11,15,16,19). Electron microscopic observation of virus particles either in thin sections of hypertrophied salivary glands or from sucrose density gradientpurified, negatively stained preparations showed enveloped bacilliform virions. In all three fly groups, the virus replicates in the salivary gland tissue of male and female flies. Additionally, infected adults do not exhibit any external disease symptoms, and morphogenesis occurs in the nuclei, resulting in nuclear SGH.The most thoroughly studied SGH viruses (SGHVs) are those associated...