title: Immune activation in the pathogenesis of treated chronic HIV disease: a workshop summary.
abstract: With the advent of highly effective antiretroviral therapy (ART), infection with human immunodeficiency virus (HIV) has become a chronic disease rather than a death sentence. Nevertheless, effectively treated individuals have a higher than normal risk for developing noninfectious comorbidities, including cardiovascular and renal disease. Although traditional risk factors of aging as well as treatment toxicity contribute to this risk, many investigators consider chronic HIV-associated inflammation a significant factor in such end-organ disease. Despite effective viral suppression, chronic inflammation persists at levels higher than in uninfected people, yet the stimuli for the inflammation and the mechanism by which inflammation persists and promotes disease pathology remain incompletely understood. This critical gap in scientific understanding complicates and hampers effective decision making about appropriate medical intervention. To better understand the mechanism(s) of chronic immune activation in treated HIV disease, three questions need answers: (1) what is the cause of persistent immune activation during treated HIV infection, (2) what are the best surrogate markers of chronic immune activation in this setting, and (3) what therapeutic intervention(s) could prevent or reverse this process? The NIH sponsored and convened a meeting to discuss the state of knowledge concerning these questions and the best course for developing effective therapeutic strategies. This report summarizes the findings of that NIH meeting.
authors.affiliation: Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. splaeger@niaid.nih.gov
authors.forename: Susan F
authors.initials: SF
authors.lastname: Plaeger
authors.forename: Brenda S
authors.initials: BS
authors.lastname: Collins
authors.forename: Runa
authors.initials: R
authors.lastname: Musib
authors.forename: Steven G
authors.initials: SG
authors.lastname: Deeks
authors.forename: Sarah
authors.initials: S
authors.lastname: Read
authors.forename: Alan
authors.initials: A
authors.lastname: Embry
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D000818:Animals; D019380:Anti-HIV Agents / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology*; D007674:Kidney Diseases / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D008213:Lymphocyte Activation / Q000276:immunology*; D011323:Primates; D012307:Risk Factors; D016097:Simian Acquired Immunodeficiency Syndrome / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents