MUMPS is considered a relatively benign childhood disease, although complications such as benign meningitis, meningoencephalitis, orchitis, pancreatitis, and neuritis may occur. The incidence of these complications varies, but most observers agree that meningoencephalitis is relatively common, whereas orchitis is almost never found before puberty. Until recently, a killed mumps virus vaccine and hyperimmune mumps γ-globulin were the only agents available to modify or prevent the disease. A major drawback of the killed vaccine is its short period of protection. Hyperimmune mumps γ-globulin was used during a recent epidemic among Eskimos in Alaska, but appeared to be ineffective.1
In 1963, Buynak and Hilleman selected a live mumps virus strain2 (Jeryl Lynn) and attenuated it by multiple passages in eggs and chick embryo cell cultures. From this strain, lots 136 and 137 were selected for a trial as a live virus vaccine.3 Lot 137 was found to be superior and during