ABSTRACT
Congenital rubella is a persistent infection that contrasts with acute postnatal infection. Basis of the Rubella virus (RV) persistence still remain unknown, though several hypotheses have been postulated. RV induces apoptosis in cell lines, maybe as a way of cell-autonomous defense mechanism against virus. Considering the pattern of c-oncogenes expression during embryogenesis, which promotes proliferation while it inhibits apoptosis in specific cells, at certain times, it can be proposed that when RV infection establishes early in gestation, embryo cells that are proliferating have their apoptotic pathways shut down; then infected proliferating embryo cells cannot execute their apoptotic death program. We here report that RV induces apoptosis in human normal-term placenta chorionic villi explants (CVE) and in monolayers of cytotrophoblasts (CTB), but does not induce apoptosis in primary human embryo fibroblasts (HEF) cultures. These results suggest distinct responses to RV infection when comparing differentiated cells, as CTB, to cells with high proliferating potential, as HEF. RV shoots apoptosis in the former, whereas in fibroblastic dividing cells derived from embryo, RV appears not to be enough stimulus to activate the genetic program of cell death.
