The placenta is a highly specialized organ that is formed during human gestation for conferring protection and generating an optimal microenvironment to maintain the equilibrium between immunological and biochemical factors for fetal development. Diverse pathogens, including viruses, can infect several cellular components of the placenta, such as trophoblasts, syncytiotrophoblasts and other hematopoietic cells. Viral infections during pregnancy have been associated with fetal malformation and pregnancy complications such as preterm labor. In this minireview, we describe the most recent findings regarding virus-host interactions at the placental interface and investigate the mechanisms through which viruses may access trophoblasts and the pathogenic processes involved in viral dissemination at the maternal-fetal interface.

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Zika virus (ZIKV) infections have been associated with severe clinical outcomes, including neurological manifestations, especially in newborns with intrauterine infection. However, no licensed vaccines or specific antiviral agents are available yet. Therefore, safe and low-cost therapy is required, especially for pregnant women. In this sense, metformin, an FDA-approved drug used to treat gestational diabetes, has previously exhibited an effect anti-ZIKA in vitro in HUVEC cells by activating AMPK. In this study, we evaluated metformin treatment during in vitro ZIKV infection in a permissive trophoblast cell line JEG3. Our results demonstrate that metformin impacts viral replication and protein synthesis and reverts the cytoskeletal changes promoted by ZIKV infection. Beyond this, lipid droplet formation is reduced, which is associated with the lipogenic activation of infection. Taken together, our findings indicate that metformin has potential as an antiviral agent against in vitro ZIKV infection in trophoblastic cells.