Background/Purpose: due to disease characteristics and treatment approaches, systemic lupus erythematosus (SLE) patients are at high risk of opportunistic virus infections, as for example Epstein Barr virus (EBV) and human cytomegalovirus (hCMV). These viruses may complicate disease course, mimic SLE manifestations and have also been involved in SLE pathogenesis. An integrated clinical, virological and immunological monitoring may allow early diagnosis, characterization and right treatment of SLE patients. Aim of our study is to analyze the prevalence of both EBV and hCMV opportunistic infections in SLE and their relationship with disease characteristics/activity

Methods: from 2/15/2013, after ethical committee approval and informed consent collection, adults SLE patients (1997 ACR classification criteria) referring consecutively to our Lupus Unit have been enrolled in this study. Quantification of EBV DNA and CMV DNA in blood was performed by real-time PCR. Detailed information regarding demographic characteristics and clinical data  (disease duration, SLEDAI 2k score, occurrence of kidney involvement, etc) were obtained from the patients’ medical records. Patients were stratified according to the degree of pharmacological immunosuppression (Group 1= hydroxychloroquine and/or prednisone≤5 mg/day; group 2= methotrexate/azathioprine/cyclosporine and/or prednisone>5 and <12.5 mg/day; group 3= mycophenolate mofetil/rituximab and/or prednisone≥12.5 mg/day)

Results: a total of 64 SLE patients (59 females/5 males) have been analyzed (table 1). Group 1 consisted of 20 patients,  group 2 of 19 patients and group 3 of 25 patients. Although no patients were suspected for viral infection, 27 (42.2%) patients had detectable DNA either of EBV (n=24) or hCMV (n=1) or both (n=2). Viral load was generally low. Patients’ age, disease duration, SLEDAI 2k score and kidney involvement did not significantly influenced viral DNA load. In group 2, detection of viral DNA was significantly higher than group 3 (p=0.0136), while no differences were observed between group 1 and 2 (p=0.3406) and group 1 and 3 (p=0.2047). Group 2 patients with detectable virus DNA (n=12) were mainly on methotrexate (n=8) and cyclosporine (n=3)

Conclusion: in our patients  a high prevalence of EBV DNA and, to a lesser extent, hCMV DNA in blood has been observed. Detection of viral DNA is not related to disease and patients characteristics. However, patients treated with methotrexate and cyclosporine (group 2), were more prone to have viral DNA load with respect to patients treated with mycophenolate mofetil, rituximab or high dose corticosteroids.  Our results suggest suggested the need of a careful monitoring of SLE patients for the increased risk of EBV and hCMV infections. Analyses to better understand how virus-specific immune responses relate to opportunistic viral infections in SLE patients are ongoing