inson for assisting us with developing a search strategy for the systematic review.


1. Introduction {#sec1-viruses-11-00706}
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Pigs of all ages are susceptible to porcine reproductive and respiratory syndrome virus (PRRSV). The clinical presentation of PRRS varies greatly between herds and can range from asymptomatic to devastating disease \[[@B1-viruses-11-00706]\]. In gilts and sows, PRRSV infection can cause reproductive failure particularly in early and late gestation, when the virus has the ability to cross the placental wall and infect the embryos. Pregnancy in pigs lasts for 114--116 days. Embryos dead prior to implantation are generally resorbed, and sows return to estrus. Embryos are also probably resorbed when death occurs between 14 and 35 days of gestation, causing irregular return to estrus if all embryos die or small litters if some of the embryos survive \[[@B2-viruses-11-00706]\]. The more severe clinical manifestation of PRRSV occurs in late gestation and is characterized by abortions (up to a 40% abortion rate in late-pregnancy sows); early farrowings; fetal death; and the birth of weak, congenitally infected piglets, resulting in elevated preweaning mortality \[[@B3-viruses-11-00706]\]. The formation of mummies, which is characteristic of PRRSV late-term infection, occurs by exsiccation of a dead fetus. Besides reproductive failure, clinical signs in pregnant sows and gilts are often mild or absent.

The mechanisms of transplacental infection and why virus transmission is blocked midpregnancy are still unclear. Pigs develop an incomplete diffuse epitheliochorial placenta without invasion. Neither the invasion of fetal tissue into the maternal endometrium nor endometrial decidualization occurs, leaving a clear distinction between maternal and fetal tissues. In pigs, maternal and fetal blood is separated by six layers of tissue (maternal endothelium, endometrial connective tissue, uterine epithelium, trophoblast, fetal placental mesenchyme, and fetal endothelium), which form a fi