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