HIV-1 persistence in the central nervous system: viral and host determinants during antiretroviral therapy

Abstract

Despite remarkable therapeutic advances in the past two decades, the elimination of human immunodeficiency virus type 1 (HIV-1) from latent reservoirs constitutes a major barrier to eradication and preventing neurological disease associated with HIV/AIDS. Invasion of the central nervous system (CNS) by HIV-1 occurs early in infection, leading to viral infection and productive persistence in brain macrophage-like cells (BMCs) including resident microglia and infiltrating macrophages. HIV-1 persistence in the brain and chronic neuroinflammation occur despite effective treatment with antiretroviral therapy (ART). This review examines the evidence from clinical studies, in vivo and in vitro models for HIV-1 CNS persistence, as well as therapeutic considerations in targeting latent CNS reservoirs.