Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood

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...

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Main Authors: Moon, Uk Yeol, Park, Su Jin, Oh, Sang Taek, Kim, Wan-Uk, Park, Sung-Hwan, Lee, Sang-Heon, Cho, Chul-Soo, Kim, Ho-Youn, Lee, Won-Keun, Lee, Suk Kyeong
Format: Online
Language:English
Published: BioMed Central 2004
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC464871/
id pubmed-464871
recordtype oai_dc
spelling pubmed-4648712004-07-16 Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood Moon, Uk Yeol Park, Su Jin Oh, Sang Taek Kim, Wan-Uk Park, Sung-Hwan Lee, Sang-Heon Cho, Chul-Soo Kim, Ho-Youn Lee, Won-Keun Lee, Suk Kyeong Research Article 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 μg PBMC DNA versus 30 ± 29 EBV genome copies/3 μg 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. BioMed Central 2004 2004-05-07 /pmc/articles/PMC464871/ /pubmed/15225364 http://dx.doi.org/10.1186/ar1181 Text en Copyright © 2004 Moon et al.; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Moon, Uk Yeol
Park, Su Jin
Oh, Sang Taek
Kim, Wan-Uk
Park, Sung-Hwan
Lee, Sang-Heon
Cho, Chul-Soo
Kim, Ho-Youn
Lee, Won-Keun
Lee, Suk Kyeong
spellingShingle Moon, Uk Yeol
Park, Su Jin
Oh, Sang Taek
Kim, Wan-Uk
Park, Sung-Hwan
Lee, Sang-Heon
Cho, Chul-Soo
Kim, Ho-Youn
Lee, Won-Keun
Lee, Suk Kyeong
Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
author_facet Moon, Uk Yeol
Park, Su Jin
Oh, Sang Taek
Kim, Wan-Uk
Park, Sung-Hwan
Lee, Sang-Heon
Cho, Chul-Soo
Kim, Ho-Youn
Lee, Won-Keun
Lee, Suk Kyeong
author_sort Moon, Uk Yeol
title Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
title_short Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
title_full Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
title_fullStr Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
title_full_unstemmed Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
title_sort patients with systemic lupus erythematosus have abnormally elevated epstein–barr virus load in blood
description 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 μg PBMC DNA versus 30 ± 29 EBV genome copies/3 μg 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.
publisher BioMed Central
publishDate 2004
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC464871/
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