11 research outputs found
Single-cycle viral gene expression, rather than progressive replication and oncolysis, is required for VSV therapy of B16 melanoma
Dynamics and mechanisms of clonal expansion of HIV-1-infected cells in a humanized mouse model
Dendritic cells efficiently transmit HIV to T Cells in a tenofovir and raltegravir insensitive manner
Time course of cellular HIV-DNA and low-level HIV viremia in HIV–HCV co-infected patients whose HCV infection had been successfully treated with directly acting antivirals
Secondary lymphoid organ fibroblastic reticular cells mediate trans-infection of HIV-1 via CD44-hyaluronan interactions
Despite early antiretroviral therapy effector memory and follicular helper CD4 T cells are major reservoirs in visceral lymphoid tissues of SIV-infected macaques
Cellular Determinants of HIV Persistence on Antiretroviral Therapy
International audienceThe era of antiretroviral therapy has made HIV-1 infection a manageable chronic disease for those with access to treatment. Despite treatment, virus persists in tissue reservoirs seeded with long-lived infected cells that are resistant to cell death and immune recognition. Which cells contribute to this reservoir and which factors determine their persistence are central questions that need to be answered to achieve viral eradication. In this chapter, we describe how cell susceptibility to infection, resistance to cell death, and immune-mediated killing as well as natural cell life span and turnover potential are central components that allow persistence of different lymphoid and myeloid cell subsets that were recently identified as key players in harboring latent and actively replicating virus. The relative contribution of these subsets to persistence of viral reservoir is described, and the open questions are highlighted