Abstract
Sir, despite the association between Epstein–Barr virus infection and multiple sclerosis being supported by an increasing number of epidemiological, serological and immunological studies (Ascherio and Munger, 2010; Maghzi et al. , 2011; Pender, 2011), the mechanisms linking increased immune reactivity to this ubiquitous herpes virus to CNS pathology in patients with multiple sclerosis remain to be demonstrated (Lunemann and Munz, 2009; Giovannoni, 2011). A point of contention is whether an active and persistent Epstein–Barr virus infection in the CNS of patients with multiple sclerosis may sustain a detrimental immunopathological response (Pender, 2009; Ascherio and Bar-Or, 2010). In support of this scenario, we have shown high frequencies of Epstein–Barr virus latently infected B cells and more sporadic signs of viral reactivation in post-mortem brain tissue from patients with multiple sclerosis but not patients with other inflammatory neurological diseases (Serafini et al. , 2007, 2010; Aloisi et al. , 2010). Presence of Epstein–Barr virus latently infected cells in active multiple sclerosis brain lesions has been confirmed recently (Tzartos et al. , 2012). In contrast, other groups did not find Epstein–Barr virus in all or the majority of post-mortem multiple sclerosis brain samples analysed (Hilton et al. , 1994; Opsahl and Kennedy, 2007; Willis et al. , 2009; Peferoen et al. , 2010; Sargsyan et al. , 2010; Torkildsen et al. , 2010). As recently discussed in Brain (Lassmann et al. , 2011), no consensus has been reached on technical and interpretation issues relating to the detection of Epstein–Barr virus in the multiple sclerosis brain. Although a variety of techniques [ in situ hybridization for Epstein–Barr virus-encoded small RNA (EBER), immunohistochemistry for Epstein–Barr virus latent and lytic proteins and PCR assays for Epstein–Barr virus nucleic acids] have been used to search …
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