The involvement of survival signaling pathways in rubella-virus induced apoptosis

Cooray, Samantha; Jin, Li; Best, Jennifer M

RV infection usually causes mild disease with few complications. However, infection during the first trimester of pregnancy results in fetal infection, and in more than 75% of cases this leads to the development of congenital abnormalities. These abnormalities include sensorineural deafness, mental retardation, and congenital heart defects, and are collectively termed congenital rubella syndrome (CRS) [5] . The cellular mechanisms activated by RV, which lead to the disruption of organogenesis, are not fully understood. However, in permissive cell cultures, the cytopathic effect (CPE) of RV has been shown to be due to caspase-dependent apoptosis [6] [7] [8] [9] [10] [11] [12] . Apoptosis is a key component of developmental processes in mammals, which functions to delete vestigial structures, control cell number and remodel tissues and organs [13] . Thus, it has been proposed that RV-induced apoptosis may cause irreparable damage to fetal tissues, resulting in the abnormalities observed in CRS [12] . However, the outcome of RV infection is likely to depend on multiple signaling events that control the balance between cell death and cell survival.