RT Journal Article
SR Electronic
T1 Experimental Zika Virus Infection in the Pregnant Common Marmoset Induces Spontaneous Fetal Loss and Neurodevelopmental Abnormalities
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 259317
DO 10.1101/259317
A1 Maxim Seferovic
A1 Claudia Sánchez-San Martín
A1 Suzette D. Tardif
A1 Julienne Rutherford
A1 Eumenia C.C. Castro
A1 Tony Li
A1 Vida L. Hodara
A1 Laura M. Parodi
A1 Luis Giavedoni
A1 Donna Layne-Colon
A1 Manasi Tamhankar
A1 Shigeo Yagi
A1 Calla Martyn
A1 Kevin Reyes
A1 Melissa Suter
A1 Kjersti M. Aagaard
A1 Charles Y. Chiu
A1 Jean L. Patterson
YR 2018
UL http://biorxiv.org/content/early/2018/02/04/259317.abstract
AB 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.