Patients with SLE have abnormally elevated Epstein-Barr virus load in blood

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Arthritis Research & Therapy

7 May 2004

Research article

Patients with systemic lupus erythematosus have abnormally elevated

Epstein-Barr virus load in blood

Uk Yeol Moon* 1 , Su Jin Park* 1 , Sang Taek Oh1 , Wan-Uk Kim2 ,

Sung-Hwan Park2 , Sang-Heon Lee2 , Chul-Soo Cho2 , Ho-Youn Kim2 ,

Won-Keun Lee3 and Suk Kyeong Lee1

1Research Institute of Immunobiology, Catholic Research Institutes of

Medical Science, Catholic University of Korea, Seoul, Korea

2Department of Medicine, The Center for Rheumatic Diseases, Kangnam St.

's Hospital, Seoul, Korea

3Department of Biological Sciences, Myongji University, Yongin,

Kyunggi-do, Korea

Abstract

Various genetic and environmental factors appear to be involved in

systemic lupus erythematosus (SLE). Epstein-Barr virus (EBV) is among

the environmental factors that are suspected of predisposing to SLE,

based on the characteristics of EBV itself and on sequence homologies

between autoantigens and EBV antigens. In addition, higher titers of

anti-EBV antibodies and increased EBV seroconversion rates have been

observed in SLE patients as compared with healthy control individuals.

Serologic responses do not directly reflect EBV status within the body.

Clarification of the precise status of EBV infection in SLE patients

would help to improve our understanding of the role played by EBV in

this disease. In the present study we determined EBV types in SLE

patients (n = 66) and normal control individual (n = 63) by direct PCR

analysis of mouthwash samples. We also compared EBV load in blood

between SLE patients (n = 24) and healthy control individuals (n = 29)

using semiquantitative PCR assay. The number of infections and EBV type

distribution were similar between adult SLE patients and healthy control

individuals (98.5% versus 94%). Interestingly, the EBV burden in

peripheral blood mononuclear cells (PBMCs) was over 15-fold greater in

SLE patients than in healthy control individuals (mean ± standard

deviation: 463 ± 570 EBV genome copies/3 ?g PBMC DNA versus 30 ± 29 EBV

genome copies/3 ?g PBMC DNA; P = 0.001), suggesting that EBV infection

is abnormally regulated in SLE. The abnormally increased proportion of

EBV-infected B cells in the SLE patients may contribute to enhanced

autoantibody production in this disease.

http://arthritis-research.com/content/6/4/R295/abstract

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