Obesity Induces an Impaired Placental Antiviral Immune Response in Pregnant Women Infected with Zika Virus
Autor: | Anna Cláudia Calvielli Castelo Branco, Emily Araujo De Oliveira, Nátalli Zanete Pereira, Ricardo Wesley Alberca, Amaro Nunes Duarte-Neto, Luiz Fernando Ferraz Da Silva, Fernanda Guedes Luiz, Naiura Vieira Pereira, Mirian Nacagami Sotto, Naiara Naiana Dejani, Patrícia Helen Carvalho Rondó, Elyzabeth Avvad-Portari, Zilton Farias Meira De Vasconcelos, Alberto José da Silva Duarte, Tamiris Azamor, Maria Notomi Sato |
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Jazyk: | angličtina |
Rok vydání: | 2023 |
Předmět: | |
Zdroj: | Viruses, Vol 15, Iss 2, p 320 (2023) |
Druh dokumentu: | article |
ISSN: | 15020320 1999-4915 |
DOI: | 10.3390/v15020320 |
Popis: | Obesity 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 (São 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. |
Databáze: | Directory of Open Access Journals |
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