After Zika virus infection, IFNAR signaling in conceptus inhibits development of placental labyrinth
MONDAY, Jan. 8, 2018 (HealthDay News) — Type 1 interferons (IFNs) may mediate pregnancy complications in the context of congenital Zika virus (ZIKV) infection, according to a study published in the Jan. 5 issue of Science Immunology.
Laura J. Yockey, from the Yale University School of Medicine in New Haven, Conn., and colleagues examined the role of type 1 IFNs in limiting or mediating ZIKV disease within a model of congenital infection, observed after ZIKV infection of type I IFN receptor knockout (ifnar1−/−) dams mating with wild-type sires, resulting in fetuses with functional type 1 IFN signaling. Pregnant dams carried a mixture of fetuses that expressed or did not express IFN-α/β receptor (IFNAR) (ifnar1+/− and ifnar1−/−) within the same uterus.
The researchers found that the titer of virus replication was higher in the placenta of ifnar1−/− than ifnar1+/−. Only ifnar1+/− fetuses were resorbed after ZIKV infection during early pregnancy; ifnar1−/− littermates continued to develop. IFNAR signaling in the conceptus was found to inhibit development of the placental labyrinth, resulting in abnormal maternal-fetal barrier architecture after ZIKV infection. Exposure of midgestation human chorionic villous explants to type I IFN resulted in altered placental morphology and cytoskeletal rearrangements within the villous core; this was not seen with exposure to type III IFN.
“Our results implicate type I IFNs as a possible mediator of pregnancy complications, including spontaneous abortions and growth restriction, in the context of congenital viral infections,” the authors write.
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