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A paper by Harley et al in Nature Genetics provides an important new perspective on the mechanisms by which infection with Epstein-Barr virus (EBV) can promote autoimmunity and, in particular, systemic lupus erythematosus (SLE).1 An interest in the role of EBV in lupus pathogenesis has a long history beginning in the 1970s with observations that patients with SLE have increased titres of anti-EBV antibodies.2 Subsequent studies have strengthened the link between EBV and SLE as well as other diseases such as rheumatoid arthritis (RA) and multiple sclerosis (MS).3 To many investigators, the question has not been whether EBV infection can lead to autoimmunity but rather how since the evidence for causality appears high.
Like other autoimmune diseases, SLE is likely the outcome of an encounter of a genetically susceptible individual with an environmental trigger such as an infection. With EBV, classic epidemiology faces a major challenge since infection with this virus, a member of the herpes family, is almost invariable in the adult population.3 While the study of disease associations in children can be informative because of their lower infection rate,4 it is difficult if not impossible to sort adults into infected and uninfected bins to investigate disease associations. Furthermore, it is always possible that abnormalities that predispose to autoimmunity also predispose to infection with EBV, complicating the situation further.
Given the limitations of epidemiology, investigators have explored other mechanisms by which EBV can trigger disease. One of the …
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