Viral infections during pregnancy have long been considered benign conditions with a few notable exceptions, such as herpes virus. The recent Ebola outbreak and other viral epidemics and pandemics show how pregnant women suffer worse outcomes (such as preterm labor and adverse fetal outcomes) than the general population and non-pregnant women. New knowledge about the ways the maternal-fetal interface and placenta interact with the maternal immune system may explain these findings. Once thought to be “immunosuppressed”, the pregnant woman actually undergoes an immunological transformation, where the immune system is necessary to promote and support the pregnancy and growing fetus. When this protection is breached, as in a viral infection, this security is weakened and infection with other microorganisms can then propagate and lead to outcomes, such as preterm labor. In this manuscript, we review the major viral infections relevant to pregnancy, and offer potential mechanisms for the associated adverse pregnancy outcomes.

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Progress in our understanding of the role of the maternal immune system during healthy pregnancy will help us better understand the role of the immune system in adverse pregnancy outcomes. In this review, we discuss our present understanding of the 'immunity of pregnancy' in the context of the response to cervical and placental infections and how these responses affect both the mother and the fetus. We discuss novel and challenging concepts that help explain the immunological aspects of pregnancy and how the mother and fetus respond to infection.

IntroductionPostnatal tissue neovascularization is an important adaptation for rescue from critical ischemia and is required for sufficient blood supply to growing tumors. This process was formerly attributed to the migration and proliferation of pre-existing, fully differentiated endothelial cells (ECs) in a process called angiogenesis. Recent studies have shown that circulating bone marrow (BM)-derived endothelial progenitor cells (EPCs) are recruited to the site of tissue regeneration and substantially contribute to neovascularization and re-endothelialization after acute vascular injury. 1,2 Intravenous infusion of EPCs after ischemia was shown to improve neovascularization and cardiac function in both animal models and pilot clinical studies. Conversely, BM-derived EPCs participate in the pathogenesis of various diseases, such as cancer, retinopathy, and atherosclerosis. 2,3 Impaired recruitment of BM-derived endothelial and hematopoietic precursor cells is known to block both tumor angiogenesis and growth. 4 Injection of BM cells promotes injuryassociated retinal angiogenesis. 5 BM-derived progenitors also contribute to the formation of the microvasculature in allograft arteriosclerotic lesions. 6 Therefore, EPCs have both physiologic and pathologic roles; thus, they have been widely considered for establishing new therapeutic strategies for the treatment of angiogenesis-related diseases.The number of circulating EPCs may limit the ultimate magnitude of angiogenesis therapies and, therefore, strategies that are based on the administration of ex vivo-expanded populations of EPCs harvested from the patient's circulating blood appear promising. 7 In addition, increased recruitment and specific lodging of EPCs in ischemic tissues may constitute another therapeutic target. Likewise, mechanisms to prevent EPC homing show promise as therapeutic strategies for the treatment of excessive neovascularization. Recently, stromal cell-derived factor-1 (SDF-1), a member of the chemokine CXC subfamily, was identified as an important factor for the trafficking of EPCs to ischemic tissues; it has also been recognized as a prominent target for increasing the engraftment of progenitor cells. 8,9 SDF-1 secreted from carcinomaassociated fibroblasts promotes angiogenesis by recruiting EPCs to tumor tissue. 3 Furthermore, ␤2-integrin expressed in EPCs was shown to mediate augmentation of the homing and neovascularization capacity of EPCs in vitro and in vivo. 10 CXCR2 also increased the homing of circulating EPCs to the sites of artery injury, possibly by enhancing adhesion of EPCs to extracellular matrix coimmobilized with chemokines. 11,12 Therefore, the identification of novel, endogenous factors that lead to both the mobilization and homing of EPCs in response to tissue hypoxia is important for the understanding of the functional contribution of EPCs to postnatal neovascularization and to the establishment of new strategies for the treatment of angiogenesis-related diseases. Here, we report a novel role and underlying signali...

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