Abstract
The aim of this study was to investigate the role of renal Epstein-Barr virus (EBV) infection in the pathogenesis of lupus nephritis (LN). A total of 58 renal tissue samples from patients with LN, seven normal renal tissue samples from patients with non-glomerular hematuria and 37 renal tissue samples from patients with minimal change nephropathy were collected. The expression of EBV-latent membrane protein-1 (EBV-LMP1) and EBV-encoded RNA 1 (EBER-1) in the renal tissue was examined by immunohistochemistry (IHC) and in situ hybridization (ISH), respectively. The sera levels of anti-nuclear antibody as well as antibodies to extractable nuclear antigen in patients with LN were also measured. An equivalence test showed that the results from the IHC and the ISH analyses had strong agreement. The positive rates of renal EBER-1 and EBV-LMP1 in the LN patients were significantly higher than those of the normal and minimal change nephropathy patients (P<0.001), while no significant difference was identified between those of the normal and minimal change nephropathy groups (P>0.05). The positive rates of EBV-LMP1 and EBER-1 in the renal tissues of patients with LN were not determined to be significantly different between the relapse (immunosuppressant-treated) and initial onset (non-treated) patients, between the patients with and without concurrent infection, and among the patients with different age ranges (P>0.05). The proportion of LN patients positive for anti-Sm antibody was significantly higher in the renal EBV-positive group than in the EBV-negative group (P<0.05), while the proportions of LN patients positive for the other autoantibodies that were examined were not identified to be significantly different between these two groups (P>0.05). The present study shows that renal EBV infection may contribute to the pathogenesis of LN by inducing anti-Sm antibody production.
Highlights
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease
Of the total 102 renal tissue samples, 42 cases were identified as expressing Epstein‐Barr virus (EBV)‐LMP1, while 41 renal tissue samples were identified as expressing EBV‐encoded RNA 1 (EBER-1)
A total of 37 renal tissue samples were positive for EBV‐LMP1 and EBER-1 while 56 renal tissue samples were negative for both
Summary
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease. The etiology and pathogenesis of SLE are possibly multifactorial; the mechanism of pathogenesis has not been fully elucidated. Since Epstein‐Barr virus (EBV) was first reported by Evans et al [6] in 1971, the relevance of EBV infection in SLE has been continuously investigated. The majority of the evidence suggesting EBV infection is involved in the pathogenesis of SLE has been obtained from viral antigens, the EBV genome or serological detection in the peripheral circulation of patients with SLE [7,8,9,10,11,12,13]. The kidney is the most commonly involved organ in patients with SLE, which is subsequently named lupus nephritis (LN). To the best of our knowledge, whether renal EBV infection is involved in the pathogenesis of LN has not been reported. The renal expression of gene and protein markers of EBV in patients with LN were detected
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
