title: T cell activation and senescence predict subclinical carotid artery disease in HIV-infected women.
abstract: BACKGROUND
  Individuals infected with human immunodeficiency virus (HIV) have increased risk of cardiovascular events. It is unknown whether T cell activation and senescence, 2 immunologic sequelae of HIV infection, are associated with vascular disease among HIV-infected adults.
  
  
  METHODS
  T cell phenotyping and carotid ultrasound were assessed among 115 HIV-infected women and 43 age- and race/ethnicity-matched HIV-uninfected controls participating in the Women's Interagency HIV Study. Multivariate analyses were used to assess the association of T cell activation (CD38(+)HLA-DR(+)) and senescence (CD28(-)CD57(+)) with subclinical carotid artery disease.
  
  
  RESULTS
  Compared with HIV-uninfected women, frequencies of CD4(+)CD38(+)HLA-DR(+), CD8(+)CD38(+)HLA-DR(+), and CD8(+)CD28(-)CD57(+) T cells were higher among HIV-infected women, including those who achieved viral suppression while receiving antiretroviral treatment. Among HIV-infected women, adjusted for age, antiretroviral medications, and viral load, higher frequencies of activated CD4(+) and CD8(+) T cells and immunosenescent CD8(+) T cells were associated with increased prevalence of carotid artery lesions (prevalence ratio(lesions) associated with activated CD4(+) T cells, 1.6 per SD [95% confidence interval {CI}, 1.1-2.2]; P = .02; prevalence ratio(lesions) associated with activated CD8(+) T cells, 2.0 per SD [95% CI, 1.2-3.3]; P < .01; prevalence ratio(lesions) associated with senescent CD8(+) T cells, 1.9 per SD [95% CI, 1.1-3.1]; P = .01).
  
  
  CONCLUSIONS
  HIV-associated T cell changes are associated with subclinical carotid artery abnormalities, which may be observed even among those patients achieving viral suppression with effective antiretroviral therapy.
authors.affiliation: Department of Epidemiology and Population Health, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461, USA. rkaplan@aecom.yu.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Kaplan
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Sinclair
authors.forename: Alan L
authors.initials: AL
authors.lastname: Landay
authors.forename: Nell
authors.initials: N
authors.lastname: Lurain
authors.forename: A Richey
authors.initials: AR
authors.lastname: Sharrett
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Gange
authors.forename: Xiaonan
authors.initials: X
authors.lastname: Xue
authors.forename: Peter
authors.initials: P
authors.lastname: Hunt
authors.forename: Roksana
authors.initials: R
authors.lastname: Karim
authors.forename: David M
authors.initials: DM
authors.lastname: Kern
authors.forename: Howard N
authors.initials: HN
authors.lastname: Hodis
authors.forename: Steven G
authors.initials: SG
authors.lastname: Deeks
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000032:analysis; D000328:Adult; D058070:Asymptomatic Diseases / Q000453:epidemiology*; D018106:CD28 Antigens / Q000032:analysis; D018959:CD57 Antigens / Q000032:analysis; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology; D002340:Carotid Artery Diseases / Q000175:diagnosis / Q000453:epidemiology*; D005260:Female; D005326:Fetal Proteins; D015658:HIV Infections / Q000150:complications* / Q000276:immunology*; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D016131:Lymphocyte Subsets / Q000737:chemistry / Q000276:immunology*; D008875:Middle Aged; D020825:T-Box Domain Proteins; D013601:T-Lymphocytes / Q000737:chemistry / Q000276:immunology*; D014463:Ultrasonography; D000098908:Brachyury Protein
chemical_list: D051997:ADP-ribosyl Cyclase 1; D018106:CD28 Antigens; D018959:CD57 Antigens; D005326:Fetal Proteins; D006684:HLA-DR Antigens; D020825:T-Box Domain Proteins; D000098908:Brachyury Protein