Central role of the placenta during viral infection: Immuno-competences and miRNA defensive responses

• Published in: Biochimica et biophysica acta. Molecular basis of disease Vol. 1867; no. 10; p. 166182
• Main Authors: Zaga-Clavellina, Verónica, Diaz, Lorenza, Olmos-Ortiz, Andrea, Godínez-Rubí, Marisol, Rojas-Mayorquín, Argelia E., Ortuño-Sahagún, Daniel
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.10.2021
• Subjects: C19MC; Human placenta; Human trophoblast; Maternal-placental-fetal interface; miRNAs; Vertical infection; Human placenta; Human trophoblast; miRNAs; Vertical infection; Maternal-placental-fetal interface; C19MC
• ISSN: 0925-4439; 1879-260X
• DOI: 10.1016/j.bbadis.2021.166182

Pregnancy is a unique immunological condition in which an “immune-diplomatic” dialogue between trophoblasts and maternal immune cells is established to protect the fetus from rejection, to create a privileged environment in the uterus and to simultaneously be alert to any infectious challenge. The maternal-placental-fetal interface (MPFI) performs an essential role in this immunological defense. In this review, we will address the MPFI as an active immuno-mechanical barrier that protects against viral infections. We will describe the main viral infections affecting the placenta and trophoblasts and present their structure, mechanisms of immunocompetence and defensive responses to viral infections in pregnancy. In particular, we will analyze infection routes in the placenta and trophoblasts and the maternal-fetal outcomes in both. Finally, we will focus on the cellular targets of the antiviral microRNAs from the C19MC cluster, and their effects at both the intra- and extracellular level. •Maternal-placental-fetal interface is a highly structured and active immunomechanical barrier.•Viral infections occurring antenatally are a major cause of fetal morbidity and mortality.•Trophoblast expresses two types of receptors for viral recognition: TLRs and RLRs.•PRR-mediated antiviral defense activates NF-κB and IRF3 to control inflammatory antiviral response.•C19MC, involved in placental morphogenesis, can confer viral resistance to infection through autophagy.