Serological studies on the epizootics of abortion, premature birth, stillbirth and congenital AH syndrome observed among cattle in Japan in 1972-1975, strongly suggested that Akabane virus, a member of Simbu group of the Bunyaviridae, was the etiologic agent of the outbreaks. This view was further corroborated by the isolation of Akabane virus from naturally affected fetuses and by the experimental inoculation of pregnant cows with the virus, which induced intrauterine infection of the fetuses and congenital deformities in infected fetuses as observed in natural cases of the congenital AH syndrome. Elsewhere, seasonal occurrence of a congenital AH syndrome in calves, lambs and kids had been reported in Australia and Israel, and serologic evidence for the etiologic role of Akabane virus had also been obtained in these countries. Furthermore, congenital AH syndrome was also reproduced by inoculation of pregnant sheep and pregnant goats with Akabane virus.
　Akabane disease in cattle, sheep and goats provides an interesting model of a congenital infection, about which very little is known with respect to how the virus causes congenital abnormalities and how long the virus persists in the fetus. Studies of the disease in these animals could also have much wider implications in determining the causes of mental retardation and congenital deformities in humans and various animals.
　These findings add Akabane virus to the growing list of teratogenic viruses, and further studies are needed to elucidate the mechanism by which it causes congenital defects.
　The formalin inactivated, aluminum phosphate gel-adsorbed vaccine prepared with Akabane virus grown in cultures of hamster lung HmLu-l cells is currently being made commercially available in Japan for prophylaxis of Akabane disease.