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Maternal-fetal interface: effect of histone deacetylases on inflammatory response regulation in HIV-1 infection

Grant number: 19/22448-0
Support type:Scholarships in Brazil - Master
Effective date (Start): August 01, 2020
Effective date (End): December 31, 2021
Field of knowledge:Biological Sciences - Immunology
Principal researcher:Maria Notomi Sato
Grantee:Sarah Cristina Gozzi e Silva
Home Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

HIV infection during pregnancy under antiretroviral therapy significantly reduced vertical transmission of the virus. However, it raised the condition of exposed and uninfected children. Considering the maternal-fetal imprint, epigenetic changes may influence the newborn's immune response. Several histone deacetylases (HDACs) may be related to the maintenance of viral latency and the use of inhibitors has been a strategy to activate HIV latency. However, other families of HDACs are important regulators of virus infection, capable of promoting chromatin remodeling and repression of gene expression and reducing inflammatory gene transcription, noting that immunoactivation in chronic HIV-1 infection is one of the dysfunctions important in the pathogenesis of the disease. Thus, the purpose of this project is to investigate the action of histone deacetylases (HDAC-1, HDAC-3, HDAC-6 and especially sirtuin 1) in the regulation of inflammatory response and viral replication at the maternal-fetal interface in infection by HIV-1. For this, the gene and protein expression of HDACs will be analyzed in the placentas of HIV-infected mothers and umbilical cord mononuclear cells (CMN), as well as the soluble form in plasma. In addition, placental explants and umbilical cord CMNs will be cultured from uninfected control mothers, cultured in the presence of inducer and inhibitor of HDACs under lipopolysaccharide inflammatory stimulus (LPS) and infected in vitro with HIV. The results obtained in this project will contribute to a better understanding of the regulation of immunoactivation mediated by HIV-1 or protective at the maternal-fetal interface. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
GOZZI-SILVA, SARAH CRISTINA; BENARD, GIL; ALBERCA, RICARDO WESLEY; YENDO, TATIANA MINA; EMIDIO TEIXEIRA, FRANCIANE MOURADIAN; OLIVEIRA, LUANA DE MENDONCA; BESERRA, DANIELLE ROSA; PIETROBON, ANNA JULIA; DE OLIVEIRA, EMILY ARAUJO; CALVIELLI CASTELO BRANCO, ANNA CLAUDIA; DE SOUZA ANDRADE, MILENA MARY; FERNANDES, IARA GRIGOLETTO; PEREIRA, NATALLI ZANETE; LEUZZI RAMOS, YASMIM ALEFE; LIMA, JULIA CATALDO; PROVENCI, BRUNA; MANGINI, SANDRIGO; DA SILVA DUARTE, ALBERTO JOSE; SATO, MARIA NOTOMI. SARS-CoV-2 Infection and CMV Dissemination in Transplant Recipients as a Treatment for Chagas Cardiomyopathy: A Case Report. TROPICAL MEDICINE AND INFECTIOUS DISEASE, v. 6, n. 1 MAR 2021. Web of Science Citations: 0.
ALBERCA, RICARDO WESLEY; DE SOUZA ANDRADE, MILENA MARY; CALVIELLI CASTELO BRANCO, ANNA CLAUDIA; PIETROBON, ANNA JULIA; PEREIRA, NATALLI ZANETE; FERNANDES, IARA GRIGOLETTO; OLIVEIRA, LUANA DE MENDONCA; EMIDIO TEIXEIRA, FRANCIANE MOURADIAN; BESERRA, DANIELLE ROSA; DE OLIVEIRA, EMILY ARAUJO; GOZZI-SILVA, SARAH CRISTINA; LEUZZI RAMOS, YASMIM ALEFE; DE BRITO, CYRO ALVES; ARNONE, MARCELO; ORFALI, RAQUEL LEAO; AOKI, VALERIA; DA SILVA DUARTE, ALBERTO JOSE; SATO, MARIA NOTOMI. Frequencies of CD33+CD11b+HLA-DR-CD14-CD66b+and CD33+CD11b+HLA-DR-CD14+CD66b-Cells in Peripheral Blood as Severity Immune Biomarkers in COVID-19. FRONTIERS IN MEDICINE, v. 7, OCT 14 2020. Web of Science Citations: 0.
ALBERCA, RICARDO WESLEY; PEREIRA, NATALLI ZANETE; OLIVEIRA, LUANDA MARA DA SILVA; GOZZI-SILVA, SARAH CRISTINA; SATO, MARIA NOTOMI. Pregnancy, Viral Infection, and COVID-19. FRONTIERS IN IMMUNOLOGY, v. 11, JUL 7 2020. Web of Science Citations: 3.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.