The question of whether the placenta is permissive to infection with ZIKV has been challenging to resolve2. Prior to the work of Miner and colleagues3, 4, another team of investigators reported that As with any landmark study, many questions remain to be answered. Firstly, on the basis of Miner and colleagues in vivoexperimentation, a considerably higher (1,000-fold) viral load was detected in the placenta than in maternal serum3, which leads to the conclusion that ZIKV has an unusually high tropism for the placenta. Is this similarly true in humans? Secondly, unlike infection with dengue virus (a related mosquito-borne Flavivirus), following dengue virus infection, no phenotype was observed and no viral RNA was detected in the placenta of ZIKV-infected mice. Why does ZIKV but not dengue virus seem to replicate in the placenta? Using fluorescence in situhybridization, direct visualization of ZIKV RNA was observed in several trophoblast cell types (glycogen and spongiotrophoblasts)3. Of potential clinical relevance to humans, placentas from ZIKV-infected pregnant mice notably show similar vascular injury, irregular shape, reduced number of fetal capillaries and evidence of apoptosis. This finding is clinically relevant as placental insufficiency in association with IUGR among women infected with ZIKV during multiple trimesters of pregnancy has been reported, and might occur independent of the more devastating microcephaly and brain malformations10. Although purely speculative, both variation in the severity of fetal infectivity and potentially natural mediation of the disease might exist.