Tiphaine Goulenok1, Anders Boyd, Martin Larsen, Solène Fastenackels, Franck Boccara, Jean-Luc Meynard, Nabila Hadour, Assia Samri, Moïse Desvarieux, Brigitte Autran, Victor Appay, Pierre-Marie Girard, Delphine Sauce. 1. aINSERM U1135, UPMC UMRS CR7, Infections and Immunity, Université Pierre et Marie Curie- Paris 6, Hôpital Pitié Salpétrière bINSERM, UMR_S1136, Institut Pierre Louis d'Epidémiologie et de Santé Publique cAP-HP Department of Cardiology, Hôpital Saint-Antoine dUPMC University Paris 06 eINSERM UMR_S938 fAP-HP Department of Infectious and Tropical Diseases, Hôpital Saint-Antoine, Paris, France gDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, USA hINSERM U1153, Centre de recherche Epidémiologies et Biostatistique iEcole des Hautes Etudes en Santé Publique jAP-HP, Groupe Hospitalier Pitié-Salpêtrière, Laboratoire d'immunologie Cellulaire et Tissulaire, Paris, France.
Abstract
OBJECTIVES: Increased risk of cardiovascular disease in patients infected with HIV has been attributed to immune activation, inflammation, and immunosenescence, all of which are linked to chronic immune activation by viral infections, particularly cytomegalovirus (CMV). Our aim is to evaluate the impact of these atherogenic markers in HIV-infected patients who never smoked. DESIGN: Exposure-matched, cross-sectional study. METHODS: In 59 HIV-infected individuals [n = 30 undergoing ≥4 years of antiretroviral therapy (ART); n = 29 never treated with ART] and 30 age-matched HIV-negative controls, we measured the level of activation and senescence, as well as the frequency of CMV-specific T cells, on peripheral blood mononuclear cells, while examining their association with carotid intima-media thickness. Partial correlations were adjusted for age, systolic blood pressure, and nadir CD4 cell count. RESULTS: The previously described roles of T-cell activation, CMV, and immunosenescence in the atherosclerotic risk of HIV-infected patients, as assessed by carotid intima-media thickness, were not apparent in our cohort of particularly 'healthy' HIV-infected never-smokers. CONCLUSION: In HIV-infected individuals at low cardiovascular disease risk, our data show that the increased risk of carotid atherosclerosis is not associated with immunological markers described to be associated with HIV disease progression.
OBJECTIVES: Increased risk of cardiovascular disease in patients infected with HIV has been attributed to immune activation, inflammation, and immunosenescence, all of which are linked to chronic immune activation by viral infections, particularly cytomegalovirus (CMV). Our aim is to evaluate the impact of these atherogenic markers in HIV-infectedpatients who never smoked. DESIGN: Exposure-matched, cross-sectional study. METHODS: In 59 HIV-infected individuals [n = 30 undergoing ≥4 years of antiretroviral therapy (ART); n = 29 never treated with ART] and 30 age-matched HIV-negative controls, we measured the level of activation and senescence, as well as the frequency of CMV-specific T cells, on peripheral blood mononuclear cells, while examining their association with carotid intima-media thickness. Partial correlations were adjusted for age, systolic blood pressure, and nadir CD4 cell count. RESULTS: The previously described roles of T-cell activation, CMV, and immunosenescence in the atherosclerotic risk of HIV-infectedpatients, as assessed by carotid intima-media thickness, were not apparent in our cohort of particularly 'healthy' HIV-infected never-smokers. CONCLUSION: In HIV-infected individuals at low cardiovascular disease risk, our data show that the increased risk of carotid atherosclerosis is not associated with immunological markers described to be associated with HIV disease progression.
Authors: Denise C Hsu; Yi Fei Ma; Sophia Hur; Danny Li; Adam Rupert; Rebecca Scherzer; S C Kalapus; Steven Deeks; Irini Sereti; Priscilla Y Hsue Journal: AIDS Date: 2016-08-24 Impact factor: 4.177