Association between serum nitric oxide and Epstein–Barr virus in patients with systemic lupus erythematosus: a case–control study

Background Epstein–Barr virus (EBV) infection may act as an environmental trigger for induction of systemic lupus erythematosus (SLE), and nitric oxide (NO) mediates many different cell functions at sites of inflammation. Objective To explore the relative frequencies of EBV and the associations between serum NO, a proinflammatory cytokine causing vasodilatation, oedema, cytotoxicity and tissue destruction, and EBV in SLE patients. Patients and methods Thirty-eight SLE adult patients and 32 healthy controls were included in this case– control study. SLE activity was assessed by systemic lupus erythematosus disease activity index (SLEDAI). EBV immunoglobulin (Ig) G and IgM antibodies, real-time PCR for EBV (EBV-DNA) and NO levels were evaluated for all participants. Results Twenty-seven (71.1%) SLE patients were positive for EBV-DNA, with a significantly higher median level (41.75 IU/ml) compared with controls (2.5 IU/ml). Frequency of EBV IgG antibody was significantly higher in SLE patients than in controls [37/38 (97.4%) vs. 26/32 (81.25%), P =0.001]. All SLE patients and controls were negative for EBV IgM antibody. EBV IgG (median) was significantly higher in SLE patients than in controls (26.25 vs. 11.35 IU/ml). EBV-DNA-positive patients showed significantly higher SLEDAI than EBV-DNA-negative patients (31.59 ±25.4 vs. 15.73 ±24.85, respectively). Serum NO was significantly higher in SLE patients than in controls (median 65.5 vs. 17 μmol/l). NO level was significantly higher in positive EBV-DNA patients than in negative ones (81 vs. 58 μmol/l). Conclusion Adult SLE patients had higher frequencies of EBV-DNA, EBV IgG and NO levels compared with healthy controls. Exposure to EBV could be associated with the increased activity of SLE (higher SLEDAI) rather than the development of the disease, and the increased NO could be a mediator of this.