부산대학교 도서관

Global Zika virus (ZIKV) outbreaks and their link to microcephaly have raised major public health concerns. However, the mechanism of maternal-fetal transmission remains largely unknown. In this study, we determined the role of yolk sac (YS) microglial progenitors in a mouse model of ZIKV vertical transmission. We found that embryonic (E) days 6.5-E8.5 were a critical window for ZIKV infection that resulted in fetal demise and microcephaly, and YS microglial progenitors were susceptible to ZIKV infection. Ablation of YS microglial progenitors significantly reduced the viral load in both the YS and the embryonic brain. Taken together, these results support the hypothesis that YS microglial progenitors serve as "Trojan horses," contributing to ZIKV fetal brain dissemination and congenital brain defects. Author summary: ZIKV is more likely to cause fetal demise and brain malformations when the mother is infected at an early stage of pregnancy, which is the critical time window when a special type of immune cells called microglia appear in the YS and migrate to the fetal brain. YS-derived microglia are susceptible to ZIKV infection and can act as "Trojan horses" to bring ZIKV from the mother to the fetal brain. [ABSTRACT FROM AUTHOR]