title: Host response to cytomegalovirus infection as a determinant of susceptibility to coronary artery disease: sex-based differences in inflammation and type of immune response.
abstract: BACKGROUND
  Positive and negative associations between cytomegalovirus (CMV) infection and coronary artery disease (CAD) have been reported. We postulated that the susceptibility to CMV-induced CAD might relate to patterns of inflammatory and immune responses to CMV infection and that sex might have an effect on these responses.
  
  
  RESULTS
  In 151 men and 87 women being evaluated for CAD, blood samples were tested for humoral (Ab+) and cellular (Tc+) responses to CMV and for C-reactive protein (CRP). In men, an elevated CRP level was a significant determinant of CAD even after adjustment for CAD risk factors (OR, 3.1; 95% CI, 1.21 to 7. 97). CMV seropositivity was associated with elevated CRP levels on multivariate analysis (P:=0.006). In contrast, in women, CMV seropositivity was independently predictive of CAD (OR, 41.8; 95% CI, 4.12 to 423.74). CRP level in women with CAD was >25% higher than those without CAD, but the difference did not reach statistical significance. Importantly, compared with CMV Ab-/Tc- women, CAD prevalence was higher in Ab+/Tc- and Ab+/Tc+ (13% versus 68% and 64%, both P:<0.005) but not in Ab-/Tc+ women (25%). There were no differences in age, smoking, diabetes, hypertension, and hypercholesterolemia among women with different types of immune responses to CMV infection.
  
  
  CONCLUSIONS
  The mechanisms by which CMV predisposes to CAD in men and women may be different. In men, CMV appears to contribute to CAD risk, insofar as it predisposes to inflammation. In women, other mechanisms, possibly related to the type of immune response generated by the host, appear to be responsible for the proatherogenic effects of CMV.
authors.affiliation: Cardiovascular Research Institute, Washington Hospital Center, Washington, DC 20010, USA.
authors.forename: J
authors.initials: J
authors.lastname: Zhu
authors.forename: G M
authors.initials: GM
authors.lastname: Shearer
authors.forename: J E
authors.initials: JE
authors.lastname: Norman
authors.forename: L A
authors.initials: LA
authors.lastname: Pinto
authors.forename: F M
authors.initials: FM
authors.lastname: Marincola
authors.forename: A
authors.initials: A
authors.lastname: Prasad
authors.forename: M A
authors.initials: MA
authors.lastname: Waclawiw
authors.forename: G
authors.initials: G
authors.lastname: Csako
authors.forename: A A
authors.initials: AA
authors.lastname: Quyyumi
authors.forename: S E
authors.initials: SE
authors.lastname: Epstein
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000914:Antibodies, Viral / Q000097:blood; D000917:Antibody Formation / Q000276:immunology; D002097:C-Reactive Protein / Q000032:analysis; D002478:Cells, Cultured; D017023:Coronary Angiography; D003327:Coronary Disease / Q000175:diagnosis / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000175:diagnosis / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology / Q000821:virology; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000821:virology; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000821:virology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012737:Sex Factors; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology
chemical_list: D000914:Antibodies, Viral; D002097:C-Reactive Protein