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ZIKV Disrupts Placental Ultrastructure and Drug Transporter Expression in Mice

Congenital Zika virus (ZIKV) infection can induce fetal brain abnormalities. Here, we investigated whether maternal ZIKV infection affects placental physiology and metabolic transport potential and impacts the fetal outcome, regardless of viral presence in the fetus at term. Low (10 PFU-ZIKV ; low Z...

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Published in:Frontiers in immunology 2021-05, Vol.12, p.680246
Main Authors: Andrade, Cherley Borba Vieira, Monteiro, Victoria Regina de Siqueira, Coelho, Sharton Vinicius Antunes, Gomes, Hanailly Ribeiro, Sousa, Ronny Paiva Campos, Nascimento, Veronica Muller de Oliveira, Bloise, Flavia Fonseca, Matthews, Stephen Giles, Bloise, Enrrico, Arruda, Luciana Barros, Ortiga-Carvalho, Tania Maria
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Language:English
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Summary:Congenital Zika virus (ZIKV) infection can induce fetal brain abnormalities. Here, we investigated whether maternal ZIKV infection affects placental physiology and metabolic transport potential and impacts the fetal outcome, regardless of viral presence in the fetus at term. Low (10 PFU-ZIKV ; low ZIKV) and high (5x10 PFU-ZIKV ; high ZIKV) virus titers were injected into immunocompetent (ICompetent C57BL/6) and immunocompromised (ICompromised A129) mice at gestational day (GD) 12.5 for tissue collection at GD18.5 (term). High ZIKV elicited fetal death rates of 66% and 100%, whereas low ZIKV induced fetal death rates of 0% and 60% in C57BL/6 and A129 dams, respectively. All surviving fetuses exhibited intrauterine growth restriction (IUGR) and decreased placental efficiency. High-ZIKV infection in C57BL/6 and A129 mice resulted in virus detection in maternal spleens and placenta, but only A129 fetuses presented virus RNA in the brain. Nevertheless, pregnancies in both strains produced fetuses with decreased head sizes (p
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.680246