Detection of Epstein-Barr Virus and Cytomegalovirus Genome in White Blood Cells from Patients with Juvenile Rheumatoid Arthritis and Childhood Systemic Lupus Erythematosus

Abstract

The role of infectious agents in the pathogenesis of autoimmune diseases has long been a matter of debate. This study investigated the possible 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 juvenile rheumatoid arthritis (JRA) patients, 20 childhood-onset systemic lupus erythematosus (SLE) patients, and 20 age-matched normals, using polymerase chain reaction (PCR) and DNA probes. The results showed: (1) there was no difference in serum IgG anti-EBV antibody titers among three groups; (2) the EBV PCR-positive rates for JRA and SLE patients and normal controls were 5% (1/21), 10 (2/20), and 0% (0/20), respectively; (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), respectively, and (4) the HCMV-positive rate was 25% for JRA patients with steroid treatment and 33% for those without steroid treatment. It is, therefore, concluded that: (1) the data do not support the participation of 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 factors contributing to increased susceptibility to HCMV infection in JRA and SLE patients.

Serologic response to Epstein-Barr virus antigens in patients with systemic lupus erythematosus: a controlled study

“…Number of studies showed that SLE patients had higher anti-EBV response and EBV DNA burden [6][7][8][9][10][11][12][13][14].…”

Systemic lupus erythematosus in adults is associated with previous Epstein-Barr virus exposure

“…When the expected true seronegative rate in adults is ϳ5%, even a false-negative rate of only 5% in detecting seroconversion against EBV will wreak havoc with the power of a study to detect an effect that is present. This means that studies that showed a possible association (14)(15)(16), as well as those that did not (17)(18)(19), contained too few SLE patients and controls to reliably and reproducibly detect a difference. In addition, only one of the previous studies used the strategy of evaluating children and adolescents (19), which would increase the ability to detect associations.…”

“…This means that studies that showed a possible association (14)(15)(16), as well as those that did not (17)(18)(19), contained too few SLE patients and controls to reliably and reproducibly detect a difference. In addition, only one of the previous studies used the strategy of evaluating children and adolescents (19), which would increase the ability to detect associations. However, this study was also underpowered and used an anti-EBV antibody assay and EBV DNA assay technologies that were even older and less reliable.…”

Antibiotic Exposure and Juvenile Idiopathic Arthritis: A Case–Control Study

“…2,3 Environmental triggers such as viral infections have been suggested, [4][5][6] but other studies have not substantiated these findings. [7][8][9][10] One study found that hospitalization for infection in the first year of life was associated with an increased risk of developing JIA. 11 However, this study focused on hospital-based diagnoses and not on antibiotic use, thus limiting its interpretability.…”