Systemic lupus erythematosus induced by Epstein-Barr virus infection

Abstract

We report a 22-year-old woman who developed systemic lupus erythematosus (SLE) immediately after an Epstein-Barr virus (EBV)-induced mononucleosis infection. The link between these two conditions has long been suspected. The close temporal relationship, the course of the pathological events and the development of immunological changes in this case provide further evidence supporting the hypothesis that EBV infection could work as a trigger in some cases of SLE, particularly if the patient is genetically susceptible.

EBV Latent Membrane Protein 2A Induces Autoreactive B Cell Activation and TLR Hypersensitivity

“…Among the environmental risk factors, EBV is the most closely associated with SLE. SLE patients have higher titers of anti-EBV Abs than control populations (1)(2)(3)(4), and EBV infection is more common among juvenile and adult SLE patients than among control populations (5,6). Some cases of SLE appear to directly result from acute EBV infection (4,7) or reactivation of EBV (8).…”

“…SLE patients have higher titers of anti-EBV Abs than control populations (1)(2)(3)(4), and EBV infection is more common among juvenile and adult SLE patients than among control populations (5,6). Some cases of SLE appear to directly result from acute EBV infection (4,7) or reactivation of EBV (8). In addition, SLE patients have a 40-fold higher EBV viral load in peripheral blood leukocytes than control populations due to poor cytotoxic T cell (CTL) responses (9) and a higher frequency of infected B cells (10).…”

Autoimmune Disorders and Lymphomas

“…The role of EBV in the pathogenesis of lymphoma in SLE patients has not been fully investigated. An increased prevalence of EBV infection in young patients with SLE has been reported (James et al, 1997) and there are some observations that, in some cases, EBV may be a trigger of lymphomagenesis in SLE (Verdolini et al, 2002). In contrast, in a retrospective study analyzing lymphoma development in a large cohort of SLE patients, EBV positivity was found only in 17% of cases (King & Costenbader, 2007).…”

BAFF/BLyS inhibitors: A new prospect for treatment of systemic lupus erythematosus

“…This high dependency on MyD88 signaling demonstrates the important role that the innate immune system plays in balancing the immune system, based on its exquisite sensitivity to Toll signaling. Indeed, the use of anti-malarial drugs to treat lupus does have some efficacy due possibly in part to blocking some aspects of TLR signaling (61), and it is thought that an environmental infectious trigger can be one pathogenic event for lupus (62,63). It is likely that there are some patients for whom the disease is independent of T cells (mirroring the BAFF-transgenic situation), and others for whom T cells play a major contributory role to pathogenesis (such as is observed in the Lyn 2/2 mice, Lpr mice, NZB.NZW F1 mice and others).…”