Purpose of review: Systemic lupus erythematosus (SLE) is a heterogeneous human disease influenced by a complex interplay of necessary, but not individually sufficient, factors. Although many genetic and environmental factors are associated with SLE, this review will focus on the evolving evidence for key Epstein-Barr virus (EBV)-specific roles in SLE, focusing on new experimental studies published during 2009, 2010, and 2011.
Recent findings: SLE patients have a dysregulated immune response against EBV. EBV antigens exhibit structural molecular mimicry with common SLE antigens and functional molecular mimicry with critical immune-regulatory components. SLE patients, from a number of unique geographic regions, are shown to have higher rates of EBV seroconversion, especially against early EBV antigens, suggesting frequent viral reactivation. SLE patients also have increased EBV viral loads and impaired EBV-specific CD8 cytotoxic T cells, with impaired cytokine responses to EBV in lupus patients. Irregular cytokine production in plasmacytoid dendritic cells and CD69 CD4 T cells after stimulation with EBV has also been demonstrated.
Summary: Recent advances demonstrate SLE-specific serologic responses, gene expression, viral load, T-cell responses, humoral fine specificity, and molecular mimicry with EBV, further supporting potential roles for EBV in lupus etiology and pathogenesis.