NATALLI ZANETE PEREIRA
Projetos de Pesquisa
Unidades Organizacionais
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina
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- Obesity Induces an Impaired Placental Antiviral Immune Response in Pregnant Women Infected with Zika Virus(2023) BRANCO, Anna Claudia Calvielli Castelo; OLIVEIRA, Emily Araujo De; PEREIRA, Natalli Zanete; ALBERCA, Ricardo Wesley; DUARTE-NETO, Amaro Nunes; SILVA, Luiz Fernando Ferraz Da; LUIZ, Fernanda Guedes; PEREIRA, Naiura Vieira; SOTTO, Mirian Nacagami; DEJANI, Naiara Naiana; RONDO, Patricia Helen Carvalho; AVVAD-PORTARI, Elyzabeth; VASCONCELOS, Zilton Farias Meira De; DUARTE, Alberto Jose da Silva; AZAMOR, Tamiris; SATO, Maria NotomiObesity is increasing in incidence worldwide, especially in women, which can affect the outcome of pregnancy. During this period, viral infections represent a risk to the mother, the placental unit, and the fetus. The Zika virus (ZIKV) outbreak in Brazil has been the cause of congenital Zika syndrome (CZS), with devastating consequences such as microcephaly in newborns. Herein, we analyzed the impact of maternal overweight/obesity on the antiviral factors' expression in the placental tissue of Zika-infected mothers. We accessed placentas from women with and without obesity from 34 public health units (Sao Paulo) and from Zika-infected mothers with and without obesity from the Clinical Cohort Study of ZIKV pregnant women (Rio de Janeiro, Brazil). We first verified that obesity, without infection, did not alter the constitutive transcriptional expression of antiviral factors or IFN type I/III expression. Interestingly, obesity, when associated with ZIKV infection, showed a decreased transcriptional expression of RIG-I and IFIH1 (MDA-5 protein precursor gene). At the protein level, we also verified a decreased RIG-I and IRF-3 expression in the decidual placenta from the Zika-infected obese group, regardless of microcephaly. This finding shows, for the first time, that obesity associated with ZIKV infection leads to an impaired type I IFN downstream signaling pathway in the maternal-fetal interface.