作者: Sophie Allart , Hélène Martin , Claire Détraves , Jérome Terrasson , Daniel Caput
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摘要: Intrauterine transmission of human cytomegalovirus (HCMV) to the fetus following primary infection in early and late pregnancy usually results severe neurological handicaps sensorineural hearing loss with typical migrational anomalies, optic atrophy, disturbed myelination, cerebella hypoplasia, microcephaly, hydrocephaly, lissencephaly. Recently, evidences raised from phenotype p73-deficient mice show that an association may exist between expression TP53 homologous gene HCMV tropism brain, suggesting implication p73 viral persistence. In this study, we demonstrated HCMV-mediated inhibition apoptosis only occurs p73-expressing cells. Upon infection, accumulation ΔN-p73α isoforms was observed HCMV-infected p73-positive This phenomenon shown be responsible for subsequent acquired resistance infected Inhibition cells by thus contribute both virus persistency abnormal nervous cell survival. finding provides first molecular basis HCMV-associated embryonic development defects newborns.