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Association of Epstein-Barr Virus with Systemic Lupus Erythematosus – Effect Modification by Race, Age, and Cytotoxic T Lymphocyte-Associate Antigen 4 Genotype

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  • Description:
    Epstein-Barr virus (EBV) is hypothesized to play a role in the development of systemic lupus erythematosus (SLE). Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is important in regulating T cell-mediated immunity, encompassing the first line of response to viral infections, and genetic variation in CTLA-4 has been associated with SLE. This study examined the seroprevalence of EBV in a population-based study of SLE patients from the southeastern United States, and potential interactions with CTLA-4 polymorphisms were assessed. Cases comprised 230 subjects recently diagnosed as having SLE (144 African American and 86 white) from university and community-based clinics, and controls comprised 276 age-, sex-, and state-matched subjects (72 African American and 204 white) recruited from driver's license registries. Antibodies to EBV capsid antigen were determined by enzyme-linked immunosorbent assay, with results expressed as positive or negative using the international standardized ratio (ISR) (a ratio of the sample absorbance to a known standard). CTLA-4 genotypes were identified by polymerase chain reaction-based methods. In African Americans, EBV-IgA seroprevalence was strongly associated with SLE (odds ratio [OR] 5.6, 95% confidence interval [95% CI] 3.0-10.6). In whites, the modest association of SLE with EBV-IgA (OR 1.6) was modified by age, in that the strongest association was observed in those older than age 50 years (OR 4.1, 95% CI 1.6-10.4). The seroprevalence of EBV-IgM and that of EBV-IgG were not associated with SLE. Higher EBV-IgG absorbance ratios were observed in SLE patients, with a significant dose response across units of the ISR in African Americans (P < 0.0001). Allelic variation in the CTLA-4 gene promoter (-1661A/G) significantly modified the association between SLE and EBV-IgA (P = 0.03), with a stronger association among those with the -1661AA genotype. These findings suggest that repeated or reactivated EBV infection, which results in increased EBV-IgA seroprevalence and higher IgG antibody titers, may be associated with SLE, and that the CTLA-4 genotype influences immune responsiveness to EBV in SLE patients. The observed patterns of effect modification by race, age, and CTLA-4 genotype should be examined in other studies and may help frame new hypotheses regarding the role of EBV in SLE etiology. [Description provided by NIOSH]
  • Subjects:
  • Keywords:
  • ISSN:
    0004-3591
  • Document Type:
    Text
  • Genre:
    Journal Article
  • Place as Subject:
  • CIO:
    National Institute for Occupational Safety and Health (NIOSH)
  • Division:
    HELD - Health Effects Laboratory Division
  • Topic:
    Workplace Safety & Health
  • Location:
    North America
  • Volume:
    52
  • Issue:
    4
  • NIOSHTIC Number:
    nn:20026788
  • Citation:
    Arthritis Rheum 2005 Apr; 52(4):1148-1159
  • Contact Point Address:
    Christine G. Parks, Biostatistics and Epidemiology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, 1095 Willowdale Road, Morgantown, WV 26505
  • Email:
    cqp8@cdc.gov
  • Federal Fiscal Year:
    2005
  • Peer Reviewed:
    True
  • Source Full Name:
    Arthritis and Rheumatism
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:5aa53f8fa52b590478ed81d8e2c8ab2a141675c6083a7091cfb20a3ecfb7958f3484d6e529bf5f6f3188b0d1a01f4096138f353539b21021a2b1630022ee1fd3
  • Download URL:
  • File Type:
    Filetype[PDF - 99.12 KB ]
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