Varicella zoster virus infection increases the risk of developing SLE disease and the modulatory role of IL-10

Herpes zoster (HZ) is a viral infection that occurs following an initial infection with the Varicella-zoster virus (VZV), which causes chickenpox. The virus remains latent in the nerve ganglia and can reactivate due to immune weakness or disorders in infected individuals. Systemic Lupus Erythematosus (SLE) is an autoimmune disease resulting from a specific immune disorder. Simultaneous infections of VZV and SLE have been reported in the literature. Additionally, most research published on scientific platforms has only compared samples from patients with SLE to those from healthy individuals. Through these two reasons above, three groups of patient samples were analyzed in this study: the first group consisted of individuals infected with herpes zoster, the second group included individuals with SLE, and the third group comprised healthy individuals. These groups and two immune markers interleukin-10 (IL-10) and IL-23 were compared with each other. The research aims to explore the potential underlying mechanisms that may link the reactivation of VZV and the presence of SLE, focusing on immunological and inflammatory pathways. The results of this research showed an increase in infections in females compared to males in both diseases. Moreover, there were no statistically significant differences between the two diseases when measuring the concentration levels of VZV IgG in each group of study models. However, there were statistically significant differences in the concentration levels of dsDNA antibodies between the groups, despite the small number of positive samples in the HZ group. As expected, there were statistically significant differences between both disease groups and the healthy group, with a negative correlation observed between the IL10 concentration levels in the HZ group and those in the SLE group.