Signaling pathways for innate immune response against dengue virus in human lung lesions

• Grant number: 25/10554-0
• Support Opportunities: Scholarships in Brazil - Master
• Start date: July 01, 2025
• End date: June 30, 2027
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Carla Pagliari
• Grantee: Geovanna Menezes Marcoli
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 24/16449-1 - Severe dengue: transcription factors associated with the innate and adaptive immune response, inflammasome components and markers of programmed cell death. In situ evaluation in human lung lesions and correlations with immunopathogenic mechanisms., AP.R

Abstract

Arboviruses are associated with different known pathogens and have a major impact on Public Health, due to the risk of epidemics and dissemination. There are still no effective therapeutic measures for the control of arboviruses, and the mechanisms determining their severity are not fully understood. We consider it crucial to evaluate the participation of the innate and acquired immune response in tissue injury events and their determining factors. Of the different arboviruses occurring in Brazil, we intend to contribute to the understanding of the pathogenesis of Dengue by analyzing cases that result in death. The lung is considered one of the organs most affected by severe dengue. We intend to further investigate the innate immune response, considering plasmacytoid dendritic cells, macrophages and transcription factors in the antiviral response in situ in lung lesions. The following will be analyzed by 1- systematic histological study with semiquantification or quantification of the anatomopathological events involved. 2- characterization and contribution of the immune response detected in situ to the pathogenesis of lesions with research on plasmacytoid dendritic cells (CD123), macrophages, interferon (IFN) alpha and beta, IRF (interferon regulatory factor), RIG (retinoic acid-inducible gene), STING (Stimulator of Interferon Genes) and MDA5 (melanoma differentiation associated 5).