These findings also support the concept that SARS-CoV-2 infection in the presence of enhanced IFNγ levels amplifies pro-inflammatory cytokine release from placenta to cause utero-placental and/or feto-placental endothelial dysfunction, contributing to SARS-CoV-2-associated adverse pregnancy outcomes such as PTB, abruption, still birth, fetal growth restriction, and/or preeclampsia. Here, IFNG is linked to fetal growth restriction.