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New Insights about Congenital Infection by Human Cytomegalovirus: Unveiling the Role of PPARγ
Stephane Chavanas1,2,3*1Centre de Physiopathologie Toulouse Purpan, Inserm Umr 1043, Toulouse, France
2CNRS UMR 5282 Toulouse, France
3Université Paul Sabatier, Toulouse, France
- *Corresponding Author:
- Stephane Chavanas
Centre de Physiopathologie Toulouse Purpan
INSERM UMR 1043, Toulouse, France
Tel: 33-0562744539
E-mail: stephane.chavanas@inserm.fr
Received date: June 22, 2016; Accepted date: July 08, 2016; Published date: July 13, 2016
Citation: Chavanas S (2016) New Insights about Congenital Infection by Human Cytomegalovirus: Unveiling the Role of PPARγ. J Infect Dis Ther 4:288. doi:10.4172/2332-0877.1000288
Copyright: © 2016 Chavanas S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Congenital infection by human cytomegalovirus (HCMV) might result in permanent neurological sequelae, including sensorineural deafness, cerebral palsies or devastating neurodevelopmental abnormalities. Neural progenitors have been suspected to be key targets of infection, hence a number of studies have shown that HCMV is able to infect neural cells and alter their differentiation. However, little was known about the molecular and genetic bases underlying homeostatic changes in the infected progenitor. We recently disclosed that Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a transcription factor of the nuclear receptor superfamily, is a key determinant of HCMV pathogenesis in the developing brain. Using neural stem cells from human embryonic stem cells, we showed that HCMV infection strongly increases levels and activity of PPARγ in NSCs. Further in vitro experiments showed that PPARγ activity inhibits the neuronogenic differentiation of NSCs into neurons. Consistently, increased PPARγ expression was found in brain section of fetuses infected by HCMV, but not in uninfected controls, what strongly supported the in vitro data. Here we review and discuss past and recent findings on the neuropathogenesis of HCMV congenital infection.
