Does herpes simplex virus have a role in the pathogenesis of systemic lupus erythematosus in Egyptians?

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by immune mediated tissue damage affecting a wide range of organs. The pathogenesis of SLE is complex. Infectious agents, including viruses, can act as environmental triggers, inducing or promoting onset and exacerbations of autoimmune disease in genetically predisposed individuals. Viral infections may be involved in the pathogenesis of SLE. To date, there is no published data about role of herpes simplex virus (HSV) in pathogenesis of SLE in Egyptian population. This study was designed to investigate a possible role of HSV in pathogenesis of SLE and its relation to disease activity. This study included 90 SLE female patients and 83 apparently healthy age-matched female subjects. SLE disease activity was assessed using SLEDAI-2K score. Qualitative assessment of anti-HSV antibodies (HSV1/2 IgM and IgG) was performed using ELISA kits. There was no statistically significant difference in frequency of HSV1/2 IgG positive test between SLE patients (97.6%) and control subjects (94.4%). There was a statistically significant increase in frequency of HSV1/2 IgM positive test in SLE patients compared to control subjects (P < 0.001). There was no difference in the frequency of HSV1/2 IgM and HSV1/2 IgG positive test results between SLE patients with higher disease activity score (60% and 95.6%, respectively) and those with lower disease activity score (60% and 93.3%, respectively). High prevalence of HSV1/2 IgG antibodies was observed among Egyptians. The lack of significant difference in frequency of HSV1/2 IgG between SLE patients and control subjects may indicate that HSV is not involved in SLE pathogenesis. Also, HSV infection may have no role in SLE disease exacerbation due to the absence of significant difference in the frequency of HSV1/2 IgM and HSV1/2 IgG antibodies in SLE patients with higher disease activity compared to those with lower disease activity.