CNRS researcher since 2020, Fernando Real is a Brazilian researcher with master and PhD degrees by Universidade Federal de São Paulo, Brazil, being a former post-doctoral fellow in the same university and in the Institut Cochin, Paris, France. Habilitation à Diriger des Recherches (HDR) degree granted by Université Paris Cité. Fascinated about how microbes establish safe niches in host organisms, remaining silent and undetected by host immune defenses, he has been studying the mechanisms of pathogen persistence in host cells, focused on immunology and cell biology of the interplay between myeloid cells and the intracellular pathogens Leishmania spp., HIV and SARS-CoV-2.
Real F, Zhu A, Belmellat A, Sennepin A, (…), Bomsel M. S100A8-mediated metabolic adaptation controls HIV-1 persistence in macrophages in vivo. Nature Communications, 2022 doi: 10.1038/s41467-022-33401-x
Real F, Ganor Y, Bomsel M. Experimental Models to Study HIV Latency Reversal from Male Genital Myeloid Cells. Methods in Molecular Biology. HIV reservoirs 2022. doi: 10.1007/978-1-0716-1871-4_14
Real F, Capron C, Sennepin A, Arrigucci R, Zhu A, (…) Bomsel M. Platelets from cART-suppressed HIV-infected patients with poor CD4+ T cell recovery carry infectious HIV. Science Translational Medicine. 2020 doi: 10.1126/scitranslmed.aat6263
Pessoa CC, Reis LC, (...) Real F*. ATP6V0d2 controls Leishmania parasitophorous vacuole biogenesis via cholesterol homeostasis. PLoS Pathogens. 2019 Jun 14;15(6):e1007834.
Real F, Sennepin A, Ganor Y, Schmitt A, Bomsel M. Live Imaging of HIV-1 Transfer across T Cell Virological Synapse to Epithelial Cells that Promotes Stromal Macrophage Infection. Cell Reports. 2018 May 8;23(6):1794-1805. doi: 10.1016/j.celrep.2018.04.028
The Chronicity of Viral Infections [CVI] is an Emergent Team investigating the molecular and cellular mechanisms driving pathogen persistence in myeloid cells. Our goals are: i) to think about strategies to neutralize pathogens before they reach safe intracellular niches (such as the macrophage and other myeloid cells, including their hematopoietic progenitors) and also to think about how to block the pathogen spreading from these cellular niches to different cells and tissues; ii) to unveil the mechanisms of latency of intracellular pathogens, responsible for disease persistence; and iii) to contribute to the development of efficient therapeutic approaches for chronic, potentially lethal, diseases. Currently we are tackling long-term immune dysfunctions caused by HIV-1 and SARS-CoV-2 hosted by macrophages, megakaryocytes and their precursors, in order to understand these myeloid viral hideouts and ultimately devise improved therapeutic strategies against HIV/AIDS and COVID-19.