Abstract
Rubella or German measles is an infection caused by rubella virus (RV). Infection of children and adults is usually characterized by a mild exanthematous febrile illness. However, RV is a major cause of birth defects and fetal death following infection in pregnant women. RV is a teratogen and is a major cause of public health concern as there are more than 100,000 cases of congenital rubella syndrome (CRS) estimated to occur every year. Several lines of evidence in the field of molecular biology of RV have provided deeper insights into the teratogenesis process. The damage to the growing fetus in infected mothers is multifactorial, arising from a combination of cellular damage, as well as its effect on the dividing cells. This review focuses on the findings in the molecular biology of RV, with special emphasis on the mitochondrial, cytoskeleton and the gene expression changes. Further, the review addresses in detail, the role of apoptosis in the teratogenesis process.