In 1814, George Maton, first recognized that a mild illness characterized by rash, adenopathy, and little or no fever was a discrete entity. Henry Veale, in 1866, named the disease rubella. The illness attracted little attention until 1942, when Norman Gregg noticed that first-trimester maternal rubella caused serious birth defects. The full spectrum and impact of rubella embryopathy remained unclarified until rubella virus was isolated in tissue culture in 1962 by two independent groups: Parkman, Buescher, and Artenstein; and Neva and Weller. Using the new tools of the virus laboratory, many investigators concentrated on the consequences of a severe rubella epidemic in 1964, which affected approximately 1% of pregnancies. Newly recognized transient manifestations of congenital rubella infection (CRI) include neonatal thrombocytopenic purpura, hepatitis, bone lesions, and meningoencephalitis and late-emerging sequelae such as diabetes mellitus and progressive rubella panencephalitis added to the cataract, heart disease, mental retardation, and deafness previously defined as due to CRI. Sharp contrasts were documented between the patterns of virus excretion and immune response of postnatal vs. congenital rubella. Licensure and widespread distribution of attenuated rubella virus vaccines in 1969 have prevented epidemic rubella. Pockets of illness remain, even in the United States. Continued effort will be required to eliminate the rubella problem.