ReviewFrontiers in immunology2026
How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Systemic lupus erythematosus (SLE) is a chronic, complex autoimmune disease arising from the interaction of environmental triggers with a genetically susceptible host. Among environmental factors, infection with Epstein-Barr virus (EBV) has one of the strongest and most consistent epidemiological associations with SLE. Patients with SLE display higher EBV seropositivity rates, increased viral loads, and more frequent viral reactivations compared with healthy individuals. In genetically predisposed hosts, EBV can disturb immune homeostasis and contribute to the breakdown of self-tolerance, acting within a broader network of environmental influences that shape lupus pathogenesis. Despite this well-established association, the precise mechanisms linking EBV infection to lupus autoimmunity have remained incompletely understood. Recent single-cell RNA-sequencing revealed that EBV-infected B cells in SLE are transcriptionally distinct, with enhanced EBNA2-driven antigen presentation and ability to activate autoreactive CD4
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