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Identification of potential therapeutic or prognosis targets associated with monocyte exhaustion of chronically infected HIV patients

Grant number: 23/04338-8
Support Opportunities:Scholarships in Brazil - Doctorate (Direct)
Effective date (Start): January 01, 2024
Effective date (End): April 30, 2028
Field of knowledge:Biological Sciences - Immunology - Applied Immunology
Principal Investigator:Fabiani Gai Frantz
Grantee:Marcelo Silva Folhas Damas
Host Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:18/15066-0 - Epigenetic programming during chronic infectious diseases: tiring out and training the innate immune system, AP.JP2


HIV is a retrovirus that currently infects about 40 million people. Combined antiretroviral therapy has increased the life expectancy and health of virus-infected patients, but has turned the infection into a chronic condition. Patients living with HIV exhibit early senescence of the innate immune system, directly related to immune exhaustion and cellular dysfunction. Extracellular vesicles (EVs) are particles released by cells in physiological situations or during infections, containing proteins, lipids, and nucleic acids representative of cellular content or metabolism. EVs are associated with intercellular communication, and our research group is particularly interested in modulating immune cell functions by EVs released during chronic infections, especially with regard to the ability to induce exhaustion and senescence phenotypes. In this regard, we are obtaining integrated proteomic and transcriptomic data from extracellular vesicles obtained from the plasma of chronically HIV-infected patients in the laboratory. In this project, an in silico analysis of this data will be performed, directed at gene and protein networks involved in inducing immune exhaustion profiles with influence from epigenetic regulation. Once the targets are identified, in vitro validation of the role of these pathways in inducing immune exhaustion phenotypes will be conducted using an immune exhaustion model. As a result, we expect to identify molecular targets that can be explored as new therapeutic or clinical progression targets.

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