Since HERV-W is expressed by a high proportion of B cells (Figure 2B), it is likely that reciprocal interactions occur within these cells during latency, that could play an additional role to the indirect mechanism proposed by Meier and coworkers, by which latent EBV infection could contribute to (neuro)inflammation, through the expression of small non-coding RNAs that bind to Toll-like receptor 3 and potentially other intracellular receptors [56]. The gene discussed is TLR3; the disease is Epstein-Barr virus infection.