Congenital rubella syndrome (CRS) can occur in children whose mothers contracted the rubella virus, sometimes called German measles, during pregnancy. Depending on the gestational period when the mother contracts rubella, an infant born with CRS may be unaffected by the virus or it may have severe developmental defects. The most severe effects of the virus on fetal development occur when the mother contracts rubella between conception and the first trimester. Defects from maternal rubella in the first trimester are included in the term congenital rubella syndrome, but physicians and researchers specifically refer to those defects as rubella embryopathy. Developmental defects are less severe if the mother contracts rubella in the second trimester, and they are generally negligible if the infection occurs in the third trimester. Prenatal rubella infection can cause birth defects which include deafness, compromised vision, abnormal heart development, and damage to the central nervous system which can lead to compromised cognition and learning disabilities.

Julia Bell worked in twentieth-century Britain, discovered Fragile X Syndrome, and helped find heritable elements of other developmental and genetic disorders. Bell also wrote much of the five volume Treasury of Human Inheritance, a collection about genetics and genetic disorders. Bell researched until late in life, authoring an original research article on the effects of the rubella virus of fetal development (Congenital Rubella Syndrome) at the age of 80.

In Australia in the 1940s, Norman McAlister Gregg observed a connection between pregnant women who contracted the rubella virus, or German measles, and cataract formation in their children's eyes. Gregg published his findings in the 1941 article Congenital Cataract following German Measles in the Mother in Transactions of the Ophthalmological Society of Australia. In the article, Gregg analyzed seventy-eight cases of congenital cataracts and suggested that the mothers' environmental factors could cause birth defects, otherwise known as teratogenic effects. Gregg's paper on the teratogenic effects of an environmental agent, the rubella virus, changed the study of birth defects to include viruses as potential causes or teratogens.

Stanley Alan Plotkin developed vaccines in the United States during the mid to late twentieth century. Plotkin began his research career at the Wistar Institute in Philadelphia, Pennsylvania, where he studied the rubella virus. In pregnant women, the rubella virus caused congenital rubella syndrome in the fetus, which led to various malformations and birth defects. Using WI-38 cells, a line of cells that originated from tissues of aborted fetuses, Plotkin successfully created RA27/3, a weakened strain of the rubella virus, which he then used to develop a rubella vaccine. Plotkin’s rubella vaccine has prevented birth defects due to congenital rubella in developing fetuses and newborns.