ArticlePLoS pathogens2016
PPARγ Is Activated during Congenital Cytomegalovirus Infection and Inhibits Neuronogenesis from Human Neural Stem Cells.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Cytomegalovirus-encoded immediate early 1 protein perturbs neural progenitor proliferation via interfering with host PML-DISC1 interaction.The Journal of biological chemistry · 2026Article
- Letermovir shows antiviral and neuroprotective effects in differentiating neurons and cerebral organoids mimicking human developing brain.Cellular and molecular life sciences : CMLS · 2026Article
- Placental Extracellular Vesicles Exhibit Reduced Neurogenic Potential Linked to Changes in Their miRNA Landscape Upon HCMV Infection.Journal of extracellular biology · 2026Article
- AAV Kills Dividing Cells by Depleting PARP1 and Other DNA Damage Response Proteins.bioRxiv : the preprint server for biology · 2025Article
- DISC1-PML protein interaction for congenital CMV infection-induced cortical neural progenitor deficit: perturbance of host signaling via viral IE1.bioRxiv : the preprint server for biology · 2025Article
- Cytomegalovirus Infection Affects the Differentiation and Determines the Functionality of a Human Progenitor Neural Cell Line.Current microbiology · 2025Article
- HCMV Infection Reduces Nidogen-1 Expression, Contributing to Impaired Neural Rosette Development in Brain Organoids.Journal of virology · 2023Article
- Fetal Brain Damage in Human Fetuses with Congenital Cytomegalovirus Infection: Histological Features and Viral Tropism.Cellular and molecular neurobiology · 2023Article
- Acute murine cytomegalovirus infection boosts cell-type specific response and lipid metabolism changes in the liver of infant mice.Frontiers in immunology · 2023Article
- Congenital cytomegalovirus infection: the state of the art and future perspectives.Frontiers in pediatrics · 2023Review
- Article
- PPAR Ligands Induce Antiviral Effects Targeting Perturbed Lipid Metabolism during SARS-CoV-2, HCV, and HCMV Infection.Biology · 2022Review
- Consequences of Viral Infection and Cytokine Production During Pregnancy on Brain Development in Offspring.Frontiers in immunology · 2022Review
- Murine Models of Central Nervous System Disease following Congenital Human Cytomegalovirus Infections.Pathogens (Basel, Switzerland) · 2021Review
- PPAR Gamma and Viral Infections of the Brain.International journal of molecular sciences · 2021Review
- Neural Stem Cells: What Happens When They Go Viral?Viruses · 2021Review
- Plasma lipidome profiling of newborns with antenatal exposure to Zika virus.PLoS neglected tropical diseases · 2021Article
- PPAR Gamma: From Definition to Molecular Targets and Therapy of Lung Diseases.International journal of molecular sciences · 2021Review
- Human Cytomegalovirus Infection Changes the Pattern of Surface Markers of Small Extracellular Vesicles Isolated From First Trimester Placental Long-Term Histocultures.Frontiers in cell and developmental biology · 2021Article
- Inhibitory effects of piceatannol on human cytomegalovirus (hCMV) in vitro.Journal of microbiology (Seoul, Korea) · 2020Article
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital infection by human cytomegalovirus (HCMV) is a leading cause of permanent sequelae of the central nervous system, including sensorineural deafness, cerebral palsies or devastating neurodevelopmental abnormalities (0.1% of all births). To gain insight on the impact of HCMV on neuronal development, we used both neural stem cells from human embryonic stem cells (NSC) and brain sections from infected fetuses and investigated the outcomes of infection on Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a transcription factor critical in the developing brain. We observed that HCMV infection dramatically impaired the rate of neuronogenesis and strongly increased PPARγ levels and activity. Consistent with these findings, levels of 9-hydroxyoctadecadienoic acid (9-HODE), a known PPARγ agonist, were significantly increased in infected NSCs. Likewise, exposure of uninfected NSCs to 9-HODE recapitulated the effect of infection on PPARγ activity. It also increased the rate of cells expressing the IE antigen in HCMV-infected NSCs. Further, we demonstrated that (1) pharmacological activation of ectopically expressed PPARγ was sufficient to induce impaired neuronogenesis of uninfected NSCs, (2) treatment of uninfected NSCs with 9-HODE impaired NSC differentiation and (3) treatment of HCMV-infected NSCs with the PPARγ inhibitor T0070907 restored a normal rate of differentiation. The role of PPARγ in the disease phenotype was strongly supported by the immunodetection of nuclear PPARγ in brain germinative zones of congenitally infected fetuses (N = 20), but not in control samples. Altogether, our findings reveal a key role for PPARγ in neurogenesis and in the pathophysiology of HCMV congenital infection. They also pave the way to the identification of PPARγ gene targets in the infected brain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.