title: HIV persistence: chemokines and their signalling pathways.
abstract: Latently infected resting CD4+ T cells are the major barrier to curing HIV. We have recently demonstrated that chemokines, which bind to the chemokine receptors CCR7, CXCR3 and CCR6, facilitate efficient HIV nuclear localisation and integration in resting CD4+ T cells, leading to latency. As latently infected cells are enriched in lymphoid tissues, where chemokines are highly concentrated, this may provide a mechanism for the generation of latently infected cells in vivo. Here we review the role of chemokines in HIV persistence; the main signalling pathways that are involved; and how these pathways may be exploited to develop novel strategies to reduce or eliminate latently infected cells.
authors: Department of Medicine, Monash University, Melbourne, 3004, Australia.
authors: Vanessa A
authors: VA
authors: Evans
authors: Gabriela
authors: G
authors: Khoury
authors: Suha
authors: S
authors: Saleh
authors: Paul U
authors: PU
authors: Cameron
authors: Sharon R
authors: SR
authors: Lewin
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D018925:Chemokines / Q000276:immunology* / Q000378:metabolism; D015658:HIV Infections / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D015497:HIV-1 / Q000276:immunology* / Q000502:physiology; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D018448:Models, Immunological; D019707:Receptors, Chemokine / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology*; D017735:Virus Latency / Q000276:immunology*
chemical_list: D018925:Chemokines; D019707:Receptors, Chemokine