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The effect of zika virus infection on placental development

Grant number: 18/07895-7
Support Opportunities:Scholarships abroad - Research Internship - Master's degree
Effective date (Start): August 27, 2018
Effective date (End): November 26, 2018
Field of knowledge:Biological Sciences - Morphology - Histology
Principal Investigator:Sonia Maria Oliani
Grantee:Rafaela Batista Molás Mendes
Supervisor: Suchita Nadkarni
Host Institution: Instituto de Biociências, Letras e Ciências Exatas (IBILCE). Universidade Estadual Paulista (UNESP). Campus de São José do Rio Preto. São José do Rio Preto , SP, Brazil
Research place: Queen Mary University of London, England  
Associated to the scholarship:17/09136-3 - Annexin A1 protein: characterization and function in placentas infected with ZIKA virus, BP.MS


Studies that allow the understanding of the mechanisms that play a role in placental pathophysiology are extremely relevant and may help to understand the many complications that compromise pregnancy and fetal health. Viral infections during pregnancy have been demonstrated to cause spontaneous abortions, stillbirth, fetal infection, intrauterine growth restriction (IUGR), preterm premature rupture of membranes and preterm delivery. ZIKV infection is strongly associated with the occurrence of microcephaly in newborns of mothers infected with this virus. When maternal viral infection does occur, it leads to productive viral replication in the placenta and a fetal inflammatory response that can have deleterious outcomes, even though the virus is not always detected in the fetus. The angiogenesis process is essential for gestational success. Vascular disorders, which can lead to decreased oxygen levels, can change placental function, impair fetal development and ultimately the health of a baby after birth. Recent studies found that the virus induces high levels of inflammation in the blood vessels of the uterus and damages placental villi, the branch-like growths that help transfer oxygen and nutrients from maternal blood to the fetus. In this study, we hypothesize that ZIKV infection could induce placental inflammation and perturb placental function and vascularization. Considering the physiological importance of blood vessels, angiogenesis, and inflammation during pregnancy, in this study we will investigate the expression and localization of VEGF, its receptors, leukocytes and the pro-angiogenic and antiinflamatory AnxA1 protein in term placentas from women infected with Zika virus. (AU)

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