Retrovirology

official impact factor 5.24

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

Open Access 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

  • * Corresponding author: Benjamin Rauwel

Author Affiliations

1 INSERM 563, Toulouse, France

2 INSERM 767, Paris, France

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Retrovirology 2009, 6(Suppl 1):O2 doi: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.