title: Multiple sclerosis: an example of pathogenic viral interaction?
abstract: A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen. Such virally induced T-cell responses might secondarily also lead to local autoimmune phenomena. Finally, research recommendations are formulated for substantiating the hypothesis on several levels: epidemiologically, genetically, and viral expression in the brain.
authors.affiliation: labormedizinisches zentrum Dr Risch, Landstr. 157, 9494, Schaan, Fürstentum, Liechtenstein. walter.fierz@risch.ch.
authors.forename: Walter
authors.identifier: 0000-0002-4192-4694
authors.initials: W
authors.lastname: Fierz
mesh_terms: D001921:Brain / Q000473:pathology / Q000821:virology; D020077:Endogenous Retroviruses / Q000472:pathogenicity*; D020031:Epstein-Barr Virus Infections / Q000150:complications*; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D015654:Herpesvirus 6, Human / Q000472:pathogenicity*; D006801:Humans; D009103:Multiple Sclerosis / Q000209:etiology*; D019349:Roseolovirus Infections / Q000150:complications*
keywords: EBNA-2; EBV; HERV-K18; HHV-6A; LMP1; MHC2TA; Multiple Sclerosis; RBPJ-kappa; Syncytin-1