TY - JOUR
T1 - Increased carotid intima-media thickness is not associated with T-cell activation nor with cytomegalovirus in HIV-infected neversmoker patients
AU - Goulenok, Tiphaine
AU - Boyd, Anders
AU - Larsen, Martin
AU - Fastenackels, Solène
AU - Boccara, Franck
AU - Meynard, Jean Luc
AU - Hadour, Nabila
AU - Samri, Assia
AU - Desvarieux, Moïse
AU - Autrana, Brigitte
AU - Appay, Victor
AU - Girard, Pierre Marie
AU - Sauce, Delphine
AU - Bastard, Jean Phillipe
AU - Capeau, Jacqueline
AU - Charbit, Beny
AU - Cohen, Ariel
AU - Demmer, Ryan T.
AU - Fellahi, Soraya
AU - Mallat, Ziad
AU - Tedgui, Alain
AU - CHIC Study group
N1 - Publisher Copyright:
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2015
Y1 - 2015
N2 - 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.
AB - 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.
KW - Atherosclerosis
KW - Cytomegalovirus
KW - HIV
KW - Immune activation
KW - Inflammation
KW - T cells
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U2 - 10.1097/QAD.0000000000000539
DO - 10.1097/QAD.0000000000000539
M3 - Article
C2 - 25686677
AN - SCOPUS:84927719148
SN - 0269-9370
VL - 29
SP - 287
EP - 293
JO - AIDS
JF - AIDS
IS - 3
ER -