An immune system mainstay in the fight against viruses may harm rather than help a pregnancy. In Zika-infected mice, this betrayal appears to contribute to fetal abnormalities linked to the virus, and it could explain pregnancy complications that arise from infections with other pathogens and from autoimmune disorders.

In pregnant mice infected with Zika virus, those fetuses with a docking station, or receptor, for immune system proteins called type I interferons either died or grew more poorly compared with fetuses lacking the receptor.