More than 30 years ago Gregg1 identified rubella virus as a cause of certain congenital defects. The discovery was important per se, since in times of rubella epidemicity the number of affected infants can be substantial. But the finding had a broader implication, for, heavy as the burden of rubella-induced defects may be, it represents only a tiny fraction of the total problem of human congenital malformation. Gregg's discovery offered hope that a major breakthrough was imminent in the identification of prenatal exposures responsible for the more prevalent malformations. That hope has not been fulfilled.A few factors — representative . . .
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Brian MacMahon (1972) studied this question.
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