Epstein-Barr Virus in Salivary Samples from Systemic Lupus Erythematosus Patients with Oral Lesions.

Alessio Buonavoglia,Gianvito Lanave,Marcella Prete,Patrizia Leone,Vito Racanelli,Lorenzo Lo Muzio,Michele Camero,Antonio Giovanni Solimando,Vito Martella,Chiara Guastadisegno

doi:10.3390/jcm10214995

Abstract

In order to investigate the possible role of Epstein–Barr virus (EBV) in systemic lupus erythematosus (SLE) and its associated oral lesions, a pilot case–control study was performed. A total of 31 patients (18 females and 13 males) were enrolled in the study and divided into two groups: group A included 16 patients with diagnosis of SLE and group B included 15 healthy individuals. Salivary swab samples were collected and subjected to molecular screening by real-time quantitative PCR (qPCR) for the detection of EBV DNA. EBV DNA was significantly detected in 8/16 (50%) SLE patients and in 5/7 (71.4%) subjects with SLE-associated oral lesions. Since EBV is one of the most common viruses in the human population, it is difficult to understand if it is the causative agent of SLE or, vice versa, if SLE is able to trigger the reactivation of EBV. This study highlights a significant association between the presence of EBV and both SLE and SLE-related oral lesions and provides rationale for further investigation into the role of EBV in SLE pathogenesis.

Highlights

In order to decipher the possible role of Epstein–Barr virus (EBV) in Systemic lupus erythematosus (SLE)-associated oral lesions, 16 SLE patients and 15 healthy individuals were enrolled in a pilot case–control study
Molecular screening by quantitative PCR (qPCR) detected EBV DNA in a total of 9/31 (29%) salivary swabs
EBV DNA positivity and a higher sero-prevalence of EBV antibodies in SLE patients compared with healthy subjects confirmed EBV reactivation [5,14,15,16,17]

Summary

Introduction

Systemic lupus erythematosus (SLE) is a chronic autoimmune rheumatic disease with unknown and unclear etiopathogenesis, with various clinical presentations, some of which are potentially life threatening [1,2,3].SLE is characterized by B and T cell dysregulation [4] and autoantibody production leading to the potential attack of any organ system [1].Skin and joints are the most commonly affected organs; kidneys with lupus nephritis, hearts with myocarditis and pericarditis, central nervous systems with cerebrovascular disease, retinae with nervous injury and potential loss of vision, muscles and lungs can be involved [1].SLE has a worldwide prevalence ranging between 12 and 50 per 100,000 individuals, with the highest incidence in individuals 40 years old and in females. Interacting with the host immune system through several mechanisms, such as structural or functional molecular mimicry [8], superantigen production [9], bystander activation [10] and epigenetic factors [11,12], EBV can cause loss of tolerance, production of autoantibodies, tissue deposition of immune complexes and consequent tissue damage [13]. These mechanisms of virus-induced autoimmunity are involved in the pathogenesis of SLE [13]. Compared with healthy subjects, SLE patients are characterized by higher EBV load, anti-EBV antibody titers and abnormal expression of viral genes [5,14,15,16,17]

Methods

Results

Conclusion