Severe fever with thrombocytopenia syndrome virus infection during pregnancy in C57/BL6 mice causes fetal damage

Background Severe fever with thrombocytopenia syndrome virus (SFTSV) is a novel tick-borne phlebovirus, which is listed in the most dangerous pathogens by the World Health Organization, and has 12-30% fatality rates. SFTSV antibodies were reported in minks that experienced abortion or reproductive failure. The aim of this study was to determine whether SFTSV infection causes an adverse pregnancy outcome in the fetus using a pregnant mouse model. Methodology/Principal findings We found SFTSV in the fetus after infection in pregnant mice, and some dams showed adverse pregnancy outcomes after infection with SFTSV including placental damage, fetal reabsorption, and fetal intrauterine growth restriction (IUGR). SFTSV had obvious tropism characteristics in the placenta, especially in the labyrinth. In early-gestation, pregnant mice infected with SFTSV had fetal IUGR and a high viral load in the fetus. The virus widely spread in infected fetuses, including the hindbrain, thymus, heart, spinal cord, and liver. Conclusions Our study demonstrated that SFTSV was vertically transmitted to the fetus through the placental barrier of immunocompetent mice, and resulted in adverse pregnancy outcomes. Author summary Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease discovered in rural areas of China in 2009, caused by a novel tick-borne phlebovirus, the SFTS virus (SFTSV). At present, SFTS reported cases are increasing, and the epidemic area of SFTSV is expanding. SFTSV is currently endemic in China, Japan, South Korea and Vietnam, and has 12-30% fatality rates. This study demonstrated that SFTSV is vertically transmitted to the fetus through the placental barrier of immunocompetent mice, and can result in fetal damage. This study highlights the possible potential impact of SFTSV on pregnant women and livestock. The results suggested that we should actively monitor the pregnancy outcomes of women and livestock infected with SFTSV, and strengthen the study of the pathogenesis of fetal damage caused by SFTSV.