This article is part of the supplement: Fifth Dominique Dormont International Conference. Host-Pathogen Interactions in Chronic Infections .

Oral presentation

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

Benjamin Rauwel¹, Bernard Mariamé¹, Hélène Martin¹, Danièle Evain-Brion², Thierry Fournier² and Christian Davrinche¹

¹  INSERM 563, Toulouse, France

²  INSERM 767, Paris, France

corresponding author email

from Fifth Dominique Dormont International Conference. Mother-to-child transmitted viral diseases: from transmission to children care
Paris, France. 26–28 March 2009

Retrovirology 2009, 6(Suppl 1):O2doi:10.1186/1742-4690-6-S1-O2

Published:	22 July 2009

First paragraph (this article has no abstract)

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.