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dc.contributor.authorSchoeman, Johannes C.
dc.contributor.authorMoutloatse, Gontse P.
dc.contributor.authorReinecke, Carools J.
dc.contributor.authorHarms, Amy C.
dc.contributor.authorVreeken, Rob J.
dc.date.accessioned2017-10-16T12:43:59Z
dc.date.available2017-10-16T12:43:59Z
dc.date.issued2017
dc.identifier.citationSchoeman, J.C. et al. 2017. Fetal metabolic stress disrupts immune homeostasis and induces proinflammatory responses in human immunodeficiency virus type 1- and combination antiretroviral therapy-exposed infants. Journal of infectious diseases, 216(4):436-446. [https://doi.org/10.1093/infdis/jix291]en_US
dc.identifier.issn0022-1899
dc.identifier.issn1537-6613 (Online)
dc.identifier.urihttp://hdl.handle.net/10394/25844
dc.identifier.urihttps://doi.org/10.1093/infdis/jix291
dc.identifier.urihttps://academic.oup.com/jid/article/216/4/436/3869800/Fetal-Metabolic-Stress-Disrupts-Immune-Homeostasis
dc.description.abstractIncreased morbidity and fetal growth restriction are reported in uninfected children born to human immunodeficiency virus type 1 (HIV-1)–infected women treated with antiretroviral (ARV) therapy. Viruses and/or pharmacological interventions such as ARVs can induce metabolic stress, skewing the cell’s immune response and restricting (cell) growth. Novel metabolomic techniques provided the opportunity to investigate the impact of fetal HIV-1 and combination ARV therapy (cART) exposure on the infants’ immune metabolome. Peroxidized lipids, generated by reactive oxygen species, were increased in cART/HIV-1–exposed infants, indicating altered mitochondrial functioning. The lipid metabolism was further dysregulated with increased triglyceride species and a subsequent decrease in phospholipids in cART/HIV-1–exposed infants compared to control infants. Proinflammatory immune mediators, lysophospholipids as well as cytokines such as CXCL10 and CCL3, were increased whereas anti-inflammatory metabolites from the cytochrome P450 pathway were reduced in cART/HIV-1–exposed infants. Taken together, these data demonstrate that the fetal metabolism is impacted by maternal factors (cART and HIV-1) and skews physiological immune responses toward inflammation in the newborn infanten_US
dc.language.isoenen_US
dc.publisherOxford Univ Pressen_US
dc.subjectImmune metabolismen_US
dc.subjectFetal developmenten_US
dc.subjectHIV-1en_US
dc.subjectMetabolomicsen_US
dc.subjectAntiretroviral therapyen_US
dc.titleFetal metabolic stress disrupts immune homeostasis and induces proinflammatory responses in human immunodeficiency virus type 1- and combination antiretroviral therapy-exposed infantsen_US
dc.typeArticleen_US
dc.contributor.researchID20212100 - Moutloatse, Gontse Panache
dc.contributor.researchID10055037 - Reinecke, Carolus Johannes
dc.contributor.researchID20382863 - Schoeman, Johannes Cornelius


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