An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus

被引:386
作者
James, JA
Kaufman, KM
Farris, AD
Taylor-Albert, E
Lehman, TJA
Harley, JB
机构
[1] Univ Oklahoma, Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA
[2] Univ Oklahoma, Hlth Sci Ctr, Dept Med, Oklahoma City, OK 73104 USA
[3] Dept Vet Affairs Med Ctr, Oklahoma City, OK 73104 USA
[4] Hosp Special Surg, New York, NY 10021 USA
关键词
autoimmunity; autoantibodies; viral infection; autoimmune disease; SLE;
D O I
10.1172/JCI119856
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
An unknown environmental agent has been suspected to induce systemic lupus erythematosus (lupus) in man. Prompted by our recent immunochemical findings, we sought evidence for an association between Epstein-Barr virus infection and lupus. Because the vast majority of adults have been infected with Epstein-Barr virus, we chose to study children and young adults, Virtually all (116 of 117, or 99%) of these young patients had seroconverted against Epstein-Barr virus, as compared with only 70% (107 of 153) of their controls (odds ratio 49.9, 95% confidence interval 9.3-1025, P < 0.00000000001). The difference in the rate of Epstein-Barr virus seroconversion could not be explained by serum IgG level or by cross-reacting anti-Sm/nRNP autoantibodies. No similar difference was found in the seroconversion rates against four other herpes viruses, An assay for Epstein-Barr viral DNA in peripheral blood lymphocytes established Epstein-Parr virus infection in the peripheral blood of all 32 of the lupus patients tested, while only 23 of the 32 matched controls were infected (odds ratio > 10, 95% confidence interval 2.53-infinity, P < 0.002), When considered with other evidence supporting a relationship between Epstein-Barr virus and lupus, these data are consistent with, but do not in themselves establish, Epstein-Barr virus infection as an etiologic factor in lupus.
引用
收藏
页码:3019 / 3026
页数:8
相关论文
共 36 条
[1]   GENETIC-STUDIES OF RO (SS-A) AND LA (SS-B) AUTOANTIBODIES IN FAMILIES WITH SYSTEMIC LUPUS-ERYTHEMATOSUS AND PRIMARY SJOGRENS SYNDROME [J].
ARNETT, FC ;
HAMILTON, RG ;
REVEILLE, JD ;
BIAS, WB ;
HARLEY, JB ;
REICHLIN, M .
ARTHRITIS AND RHEUMATISM, 1989, 32 (04) :413-419
[2]  
EVANS AS, 1971, LANCET, V1, P167
[3]  
EVANS AS, 1989, VIRAL INFECT HUMANS, P265
[4]   ACTIVATION OF EPSTEIN-BARR-VIRUS LATENT GENES PROTECTS HUMAN B-CELLS FROM DEATH BY APOPTOSIS [J].
GREGORY, CD ;
DIVE, C ;
HENDERSON, S ;
SMITH, CA ;
WILLIAMS, GT ;
GORDON, J ;
RICKINSON, AB .
NATURE, 1991, 349 (6310) :612-614
[5]   EPSTEIN-BARR VIRUS-CODED BHRF1 PROTEIN, A VIRAL HOMOLOG OF BCL-2, PROTECTS HUMAN B-CELLS FROM PROGRAMMED CELL-DEATH [J].
HENDERSON, S ;
HUEN, D ;
ROWE, M ;
DAWSON, C ;
JOHNSON, G ;
RICKINSON, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (18) :8479-8483
[6]  
James JA, 1996, J IMMUNOL, V156, P4018
[7]   Lupus humoral autoimmunity after short peptide immunization [J].
James, JA ;
Scofield, RH ;
Harley, JB .
B LYMPHOCYTES AND AUTOIMMUNITY, 1997, 815 :124-127
[8]  
JAMES JA, 1992, J IMMUNOL, V148, P2074
[9]   IMMUNOGLOBULIN EPITOPE SPREADING AND AUTOIMMUNE-DISEASE AFTER PEPTIDE IMMUNIZATION - SM B/B'-DERIVED PPPGMRPP AND PPPGIRGP INDUCE SPLICEOSOME AUTOIMMUNITY [J].
JAMES, JA ;
GROSS, T ;
SCOFIELD, RH ;
HARLEY, JB .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 181 (02) :453-461
[10]  
JAMES JA, 1994, CLIN EXP IMMUNOL, V98, P419