Latent EBV infection may contribute to neuroinflammation by triggering IFN-α production, as supported by the findings that EBERs can bind to Toll-like receptor 3 and potentially other intracellular receptors such as retinoic acid-inducible gene 1 (RIG-I) and elicit IFN-α production (31). This evidence concerns the gene IFNA1 and Epstein-Barr virus infection.