Epstein–Barr virus and systemic lupus erythematosus

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Purpose of review

Systemic lupus erythematosus is a complex human disease likely influenced by a compilation of necessary, but not individually sufficient, features. Although many genetic and environmental factors are associated, this review will focus on the evolving evidence for key Epstein–Barr virus specific roles.

Recent findings

Recent studies have shown additional molecular mimicry mechanisms between early events in lupus autoimmunity and specific Epstein–Barr virus responses. In addition, several recent papers have demonstrated increased Epstein–Barr viral load, increased numbers of latently infected peripheral B cells, impaired functional T cell responses, and association of the presence of Epstein–Barr virus DNA in systemic lupus erythematosus patients compared with controls. Additional work has continued to show association of various aspects of Epstein–Barr virus serology with systemic lupus erythematosus and a recent paper outlines differences in the pediatric systemic lupus erythematosus humoral immune response to Epstein–Barr virus nuclear antigen-1 compared with matched controls.


This review will briefly outline the recent advances that show serologic, DNA, gene expression, viral load, T cell responses, humoral fine specificity, and molecular mimicry evidence for differences between systemic lupus erythematosus patients and controls and the impact that these findings have on understanding the role of Epstein–Barr virus in systemic lupus.

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