Increased carotid intima–media thickness is not associated with T-cell activation nor with cytomegalovirus in HIV-infected never-smoker patients
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 thes...
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Published in | AIDS (London) Vol. 29; no. 3; pp. 287 - 293 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
Wolters Kluwer
28.01.2015
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Abstract | 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.
Exposure-matched, cross-sectional study.
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.
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.
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. |
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AbstractList | 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 > or =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 super(+) 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. 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. Exposure-matched, cross-sectional study. 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. 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. 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. 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.OBJECTIVESIncreased 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.Exposure-matched, cross-sectional study.DESIGNExposure-matched, cross-sectional study.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.METHODSIn 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.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.RESULTSThe 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.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.CONCLUSIONIn 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-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. |
Author | Goulenok, Tiphaine Desvarieux, Moïse Girard, Pierre-Marie Larsen, Martin Meynard, Jean-Luc Sauce, Delphine Boyd, Anders Autran, Brigitte Fastenackels, Solène Hadour, Nabila Appay, Victor Samri, Assia Boccara, Franck |
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CitedBy_id | crossref_primary_10_1007_s00430_019_00612_x crossref_primary_10_1097_COH_0000000000000241 crossref_primary_10_1016_j_clim_2017_11_001 crossref_primary_10_1097_QAD_0000000000001109 crossref_primary_10_1186_s12865_016_0175_7 crossref_primary_10_1016_j_molmed_2015_03_004 crossref_primary_10_1016_j_jacc_2017_05_012 crossref_primary_10_1016_j_intimp_2016_11_007 crossref_primary_10_1097_QAD_0000000000001149 crossref_primary_10_1186_s12865_022_00498_0 crossref_primary_10_1186_s12981_017_0180_9 crossref_primary_10_5812_numonthly_63900 |
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Keywords | Cytomegalovirus Inflammation Immune activation HIV T cells Atherosclerosis |
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References | Desvarieux (R11-4-20210130) 2005; 111 Valiathan (R18-4-20210130) 2014; 9 Larsen (R14-4-20210130) 2012; 7 Sauce (R15-4-20210130) 2011; 117 Palella (R3-4-20210130) 2011; 6 Parrinello (R9-4-20210130) 2012; 205 Appay (R7-4-20210130) 2011; 25 Currier (R1-4-20210130) 2008; 118 Sacre (R17-4-20210130) 2012; 26 Hansson (R4-4-20210130) 2005; 352 Hsue (R8-4-20210130) 2006; 20 Kaplan (R16-4-20210130) 2011; 217 Desvarieux (R10-4-20210130) 2013; 27 Andersson (R5-4-20210130) 2010; 134 Sauce (R13-4-20210130) 2009; 119 Sauce (R12-4-20210130) 2012; 189 Naeger (R6-4-20210130) 2010; 5 Boccara (R2-4-20210130) 2013; 61 |
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SubjectTerms | Adult Atherosclerosis - etiology Atherosclerosis - pathology Carotid Intima-Media Thickness Cross-Sectional Studies Cytomegalovirus Cytomegalovirus Infections - pathology Herpesviridae HIV Infections - complications HIV Infections - immunology HIV Infections - pathology Humans Immunology Lentivirus Life Sciences Male Middle Aged Retroviridae T-Lymphocytes - immunology Tunica Intima - pathology |
Title | Increased carotid intima–media thickness is not associated with T-cell activation nor with cytomegalovirus in HIV-infected never-smoker patients |
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