Previous studies that have generated animal models of human Zika virus (ZIKV) infection have need to manipulate mice to impair their type I interferon (IFN) signalling, allowing for enhanced infection and vertical transmission of virus to the embryo. The authors found that pregnant mice are actually able to generate type I IFN responses that can limit ZIKV infection, but still develop profound placental pathology and a high frequency of fetal death. They found that maternal ZIKV exposure leads to placental pathology and ZIKV RNA levels in maternal, placental or embryonic tissues are not predictive of the pathological effects seen in the embryos. The placental pathology seen included trophoblast hyperplasia in the labyrinth, trophoblast giant cell necrosis in the junctional zone and loss of embryonic vessels. This suggests that where there is limited infection, placental pathology rather than embryonic/fetal viral infection may be a stronger contributor to adverse pregnancy outcomes in mice. Therefore, in immunocompetent mice, direct viral infection of the embryo is not essential for fetal death. This immunologically unmanipulated pregnant mouse model can therefore be used to assess fetal outcome following ZIKV infection and therefore may be a model to test prophylactic and therapeutic interventions to protect the fetus during pregnancy.
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