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      Viral infection of the placenta leads to fetal inflammation and sensitization to bacterial products predisposing to preterm labor.

      The Journal of Immunology Author Choice
      Animals, Bacterial Infections, complications, immunology, microbiology, Cell Line, Cells, Cultured, Cytokines, metabolism, Female, Fetal Diseases, virology, Fetus, Host-Pathogen Interactions, Humans, Immunohistochemistry, Inflammation, etiology, Maternal-Fetal Exchange, Mice, Mice, Inbred C57BL, Mice, Knockout, NIH 3T3 Cells, Obstetric Labor, Premature, Placenta, Placenta Diseases, Pregnancy, Pregnancy Complications, Infectious, Rhadinovirus, physiology, Toll-Like Receptor 3, genetics, Virus Diseases

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          Abstract

          Pandemics pose a more significant threat to pregnant women than to the nonpregnant population and may have a detrimental effect on the well being of the fetus. We have developed an animal model to evaluate the consequences of a viral infection characterized by lack of fetal transmission. The experiments described in this work show that viral infection of the placenta can elicit a fetal inflammatory response that, in turn, can cause organ damage and potentially downstream developmental deficiencies. Furthermore, we demonstrate that viral infection of the placenta may sensitize the pregnant mother to bacterial products and promote preterm labor. It is critical to take into consideration the fact that during pregnancy it is not only the maternal immune system responding, but also the fetal/placental unit. Our results further support the immunological role of the placenta and the fetus affecting the global response of the mother to microbial infections. This is relevant for making decisions associated with treatment and prevention during pandemics.

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