title: HIV-associated lymphoma in the era of combination antiretroviral therapy: shifting the immunological landscape.
abstract: HIV infection increases the risk of many types of cancer, including lymphoma. Combination antiretroviral therapy (cART) has reduced, but not eliminated, the risk of HIV-associated lymphoma. There has been a substantial shift in the subtypes of lymphoma observed in HIV-infected patients treated with cART. In this review, we will first outline these changes based on epidemiological studies and describe the impact of cART on lymphoma risk and mortality. Then, we will discuss some immunological factors that may contribute to the increased risk of lymphoma persisting after the administration of cART, including immunological non-response to therapy, chronic B-cell activation and dysfunction, T follicular helper cells, natural killer cells and altered lymphopoiesis. A better understanding of the pathophysiologic mechanisms of HIV-associated lymphoma under effective cART will inform future treatment strategies.
authors.affiliation: Institute of Human Virology, and Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201-1009, USA vicarroll@ihv.umaryland.edu.
authors.forename: Virginia
authors.initials: V
authors.lastname: Carroll
authors.affiliation: Institute of Human Virology, and Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201-1009, USA Department of Molecular Medicine, University of Padova, Padova 35121, Italy.
authors.forename: Alfredo
authors.initials: A
authors.lastname: Garzino-Demo
mesh_terms: D044966:Anti-Retroviral Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D016483:Lymphoma, AIDS-Related / Q000453:epidemiology*
chemical_list: D044966:Anti-Retroviral Agents
keywords: HIV-1; antiretroviral drugs; chronic infection; immune activation; lymphomagenesis; virus