Research square · 2025
Nonhuman primate model mirroring human congenital cytomegalovirus infection reveals a spectrum of vertical transmission outcomes.
СтатьяПрепринтНазвание и аннотация: Перевод в очереди
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Kaur Amitinder, Manuel Tabitha, Moström Matilda, Crooks Chelsea, Davalos Angel, Barfield Richard, Scheef Elizabeth, Kendall Savannah, Midkiff Cecily, Sprehe Lesli, Trexler Macey, Boquet Francis, Shroyer Monica, Danner Victoria, Doyle-Meyers Lara, Weinbaum Carolyn, Mirza Anne, Lammi Stephen, Otero Claire, Lee Marissa, Rogers Layne, Granek Joshua, Owzar Kuoros, Malouli Daniel, Fruh Klaus, Kowalik Timothy, Chan Cliburn, Permar Sallie, Blair Robert
Аннотация
Congenital cytomegalovirus (cCMV) is the leading infectious cause of birth defects worldwide, yet immune determinants of protection to inform maternal vaccine design remain elusive due to the lack of a translational animal model. Here, we characterized the outcome of primary rhesus CMV (RhCMV) infection in pregnant, immunocompetent, CMV-naïve rhesus macaques. RhCMV DNA was detected in amniotic fluid and/or fetal tissues in six of 12 (50% placental transmission) dams following early second trimester gestation RhCMV inoculation. Widespread tissue dissemination dominated by one of two inoculated RhCMV strains was present in one fetus (8.3% cCMV disease). Placental transmission was associated with elevated fetal and maternal plasma TNF-alpha and reduced maternal brain-derived neurotrophic factor and IL-10 levels. CMV exposure during pregnancy had a broad impact on the placenta and fetus even in the absence of congenital infection, as evidenced by ubiquitous maternal-fetal interface infection, and reduced placental efficiency and small-for-gestation age fetuses compared to control pregnancies. This model recapitulates key aspects of human cCMV and provides new insights into the complexity of CMV vertical transmission.