Demonstration of microchimerism in pregnant sows and effects of congenital PRRSV infection

The presence of small numbers of foreign cells within tissues or circulation of an individual is described as microchimerism [1]. Naturally acquired microchimerism refers to sibling (exchange of fetal cells in between siblings), maternal (presence of maternal cells within fetus) and fetal microchimerism (presence of fetal cells within mother) [2-16]. Fetal and maternal cell exchange is common in human and rodent pregnancy [1]. Both fetal and maternal microchimerism has been associated with different autoimmune disorders, pregnancy pathology and transplantation complications [1,17-19]. Otherwise, fetal cell differentiation in maternal tissues is presumably involved in tissue repair and protection against cancer [1]. Microchimerism may also play an important role in the physiology and pathology of pregnancy. However, at present no information is available on this phenomenon in swine.Porcine reproductive and respiratory syndrome virus (PRRSV) is the cause of severe reproductive problems in sows [20]. The means by which PRRSV crosses the placental barrier remain unknown. Prior to fetal infection, PRRSV replicates in the endometrium and shows a very restricted tropism for Sn+/CD163+ macrophages [21,22]. Therefore, PRRSV might use susceptible cells as a vehicle to cross the uterine epithelium/trophoblast layers. Some pathological conditions during pregnancy, especially diseases that affect the placental environment, might influence fetal and maternal cell exchange. For instance, it has been observed that a mild inflammation caused by Pertussis toxin enhances cell migration through the murine placenta [23]. During replication in the endometrium, PRRSV causes apoptosis of infected and surrounding cells [22] and changes the expression of cellular receptors (increased Sn expression and change in the MHC class I and II expression) (not published results). Potentially, PRRSV-mediated changes in endometrial macrophages and/or in uterine epithelial/trophoblast layers may trigger