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Sci Rep. 2018 May 1;8(1):6851. doi: 10.1038/s41598-018-25205-1.

Experimental Zika Virus Infection in the Pregnant Common Marmoset Induces Spontaneous Fetal Loss and Neurodevelopmental Abnormalities.

Author information

1
Departments of Obstetrics and Gynecology, Molecular and Human Genetics, and Pathology and Laboratory Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, TX, 77030, USA.
2
Department of Laboratory Medicine, University of California, San Francisco, CA, 94143, USA.
3
Southwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, 78245, USA.
4
Department of Women, Children and Family Health Science, University of Illinois at Chicago, Chicago, IL, 60612, USA.
5
Department of Virology and Immunology, Texas Biomedical Research Institute, San Antonio, TX, 78245, USA.
6
California Department of Public Health, Richmond, CA, 94804, USA.
7
Departments of Obstetrics and Gynecology, Molecular and Human Genetics, and Pathology and Laboratory Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, TX, 77030, USA. aagaardt@bcm.edu.
8
Department of Laboratory Medicine, University of California, San Francisco, CA, 94143, USA. charles.chiu@ucsf.edu.
9
Department of Medicine/Infectious Diseases, University of California, San Francisco, CA, 94143, USA. charles.chiu@ucsf.edu.
10
Department of Virology and Immunology, Texas Biomedical Research Institute, San Antonio, TX, 78245, USA. jpatters@txbiomed.org.

Abstract

During its most recent outbreak across the Americas, Zika virus (ZIKV) was surprisingly shown to cause fetal loss and congenital malformations in acutely and chronically infected pregnant women. However, understanding the underlying pathogenesis of ZIKV congenital disease has been hampered by a lack of relevant in vivo experimental models. Here we present a candidate New World monkey model of ZIKV infection in pregnant marmosets that faithfully recapitulates human disease. ZIKV inoculation at the human-equivalent of early gestation caused an asymptomatic seroconversion, induction of type I/II interferon-associated genes and proinflammatory cytokines, and persistent viremia and viruria. Spontaneous pregnancy loss was observed 16-18 days post-infection, with extensive active placental viral replication and fetal neurocellular disorganization similar to that seen in humans. These findings underscore the key role of the placenta as a conduit for fetal infection, and demonstrate the utility of marmosets as a highly relevant model for studying congenital ZIKV disease and pregnancy loss.

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