Sharma V, Goessling LS, Brar AK, et al. - Given that the fetal heart shows high expression of coxsackie and adenovirus receptor, which is involved in targeting of cardiomyocytes by coxsackievirus B (CVB), researchers here examined their hypothesis that CVB3 can precipitate congenital heart defects when fetal infection occurs during critical window of gestation. Infection with CVB3 was induced in C57Bl/6 pregnant mice during time points in early gestation (embryonic day [E] 5, E7, E9, and E11). As viral exposure was made between E7 and E9, 209 examined viable fetuses exhibited characteristic features of ventricular septal defect (33.6%), abnormal myocardial architecture resembling noncompaction (23.5%), and double‐outlet right ventricle (4.4%). A direct correlation was observed between viral titers and severity of congenital heart defects, with apparent predominance among female fetuses.Overall findings suggest that congenital heart defects are induced by prenatal CVB3 infection. Most of the observed phenotypes seemed to be explained by alterations in myocardial proliferate capacity and consequent changes in cardiac architecture and trabeculation.