Lack of evidence of active lytic replication of Epstein-Barr and cytomegaloviruses in patients with systemic lupus erythematosus

Abstract

Objectives Systemic lupus erythematosus (SLE) is a multifactorial disease. Environmental factors such as viral infection(s) have been proposed as pathaetioiogical factors. There are particular interests in studying lymphotropic viruses such as the Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Although previous case reports and in vitro studies suggested that they may have a role, there is no direct evidence that onset of SLE or disease exacerbation is associated with active infection by these viruses. Using the very sensitive polymerase chain reaction (PCR) technique, we tried to find out evidence of active replication of these viruses in patients with SLE. Methods Thirty-four patients with SLE were compared with matched normal controls. Eleven patients were newly diagnosed to have SLE and 18 of the 34 patients had active disease as determined by a SLE Disease Activity Index (SLEDAI) score of ≥ 10 at the time of study. Results Our results showed no evidence of active replication or reactivation of EBV in the leucocytes amongst the newly diagnosed SLE patients, established SLE patients, patients with SLEDAI ≥ 10, patients with SLEDAI < 10, and control subjects. There was no evidence of CMV infection in any of the subjects studied. The IgG and IgA responses against EBV early antigen (EA) and viral capsid antigen (VGA) were also studied. The IgG and IgA responses against VGA of EBV were increased in patients with SLE when compared with controls. However, there were no differences in these responses among different subgroups of patients. The mechanism of these responses was not apparent but may represent non-specific hyperimmune responses in these patients. There were no differences in the titre of IgG and IgA against EBV EA between the patient groups and controls. Conclusion There is no direct evidence that either EBV or CMV plays a direct role in the onset and/or exacerbation of SLE.