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Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis
Author(s) -
Priscilla Y. Hsue,
Peter W. Hunt,
Audrey H. Schnell,
S.C. Kalapus,
Rebecca Hoh,
Patricia A. Ganz,
Jeffrey N. Martin,
Steven G. Deeks
Publication year - 2009
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0b013e32832b514b
Subject(s) - viremia , medicine , viral load , immunology , intima media thickness , inflammation , cohort , lentivirus , human immunodeficiency virus (hiv) , viral disease , carotid arteries
HIV-seropositive patients are at higher risk for atherosclerosis than HIV-seronegative persons. This has been variably attributed to antiretroviral drug toxicity, immunodeficiency, and/or HIV-associated inflammation. To evaluate the contributions of these factors to HIV-associated atherosclerosis, we assessed carotid artery intima-media thickness in a diverse cohort of HIV-seronegative and seropositive adults, including a unique group of HIV-infected patients who were untreated, had undetectable viral loads, and had preserved CD4 T-cell counts (HIV controllers).

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