Establishing The Developmental Correlates of Fetal Susceptibility to Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Infection

Porcine reproductive and respiratory syndrome virus (PRRSV) costs the American swine industry an estimated $1.2BM/year. Of this, a significant portion, is borne by the breeding herd, where PRRSV infection causes abortions and increased stillbirths/mummified fetuses. Recent work demonstrates that a significant portion of late gestation fetuses are naturally resistant to congenital infection and thereby escape the physiological and developmental disruptions which compromise viability. However, the mechanism by which PRRSV crosses the porcine placenta, remains unknown. The long-term goal of this research is to enhance fetal resistance to congenital infection, thereby minimizing the consequences of this virus in the American swine herd. To do so it is critically necessary to identify the underlying molecular mechanisms of fetal resistance to transplacental PRRSV infection. To this end, the objectives are 1) Define the point of transition from mid gestation placental resistance to late gestation placental permissibility to PRRSV infection, and 2) Characterize the role of intrauterine growth retardation (IUGR) on fetal susceptibility to infection. To accomplish these objectives, we will evaluate fetal viral load and targeted placental transcriptome following viral challenge in gilts at varying gestational ages or following unilateral oviductal ligations which suppresses naturally occurring IUGR. Outcomes of this will be 1) an improved understanding of the placenta factors associated with resistance and 2) vital preliminary data necessary to support future funding applications for the in-depth study of the molecular mechanisms underpinning vertical transmission and fetal resistance to infection. Program Area Priority: Cellular, molecular, genomic/genetic or whole-animal aspects of animal health and disease