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Human cytomegalovirus (HCMV) contributes to pathogenic processes in immuno-suppressed individuals, in fetuses and in neonates. Infection during pregnancy is known to cause miscarriages and low-birthweight newborns and we know that in this case infection of the placenta precedes transmission to the fetus. HCMV was shown to benefit from inflammatory conditions by using the cyclooxygenase-2 (Cox-2)-dependent prostaglandin pathway for transcription of the essential immediate-early gene IE2. The fact that Cox-2 activation could serve as a source of ligand for the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), which is known to play a pivotal role in controlling human trophoblast invasion, led us to hypothesize that HCMV could impair placentation through activation of PPARγ.

Activation of PPARγ by human CMV for de novo replication impairs invasiveness of cytotrophoblast from early placenta