DETECTION OF EPSTEIN-BARR-VIRUS AND CYTOMEGALOVIRUS GENOME IN WHITE BLOOD-CELLS FROM PATIENTS WITH JUVENILE RHEUMATOID-ARTHRITIS AND CHILDHOOD SYSTEMIC LUPUS-ERYTHEMATOSUS

Citation
Yt. Tsai et al., DETECTION OF EPSTEIN-BARR-VIRUS AND CYTOMEGALOVIRUS GENOME IN WHITE BLOOD-CELLS FROM PATIENTS WITH JUVENILE RHEUMATOID-ARTHRITIS AND CHILDHOOD SYSTEMIC LUPUS-ERYTHEMATOSUS, International archives of allergy and immunology, 106(3), 1995, pp. 235-240
Citations number
32
Categorie Soggetti
Allergy,Immunology
ISSN journal
10182438
Volume
106
Issue
3
Year of publication
1995
Pages
235 - 240
Database
ISI
SICI code
1018-2438(1995)106:3<235:DOEACG>2.0.ZU;2-C
Abstract
The role of infectious agents in the pathogenesis of autoimmune diseas es has long been a matter of debate. This study investigated the possi ble role of Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) infections in the pathogenesis of autoimmune diseases by an attempt to demonstrate the presence of the viral genome in the leukocyte of 21 j uvenile rheumatoid arthritis (JRA) patients, 20 childhood-onset system ic lupus erythematosus (SLE) patients, acid 20 age-matched normals, us ing polymerase chain reaction (PCR) and DNA probes. The results showed : (1) there was no difference in serum IgG anti-EBV antibody titers am ong three groups; (2) the EBV PCR-positive rates for JRA and SLE patie nts and normal controls were 5% (1/21), 10 (2/20), and 0% (0/20), resp ectively; (3) the HCMV PCR-positive rates for JRA and SLE patients and normal controls were 33% (7/21), 25 (5/20), and 10% (2/20), respectiv ely, and (4) the HCMV-positive rate was 25% for JRA patients with ster oid treatment and 33% for those without steroid treatment. It is, ther efore, concluded that: (1) the data do not support the participation o f EBV and HCMV in the pathogenesis of childhood-onset SLE and JRA; (2) steroid therapy does not increase the frequency of HCMV infection in JRA patients, and (3) immunoincompetence might be one of the major fac tors contributing to increased susceptibility to HCMV infection in JRA and SLE patients.