Description:
The triggers for the development of multiple sclerosis (MS) have not been fully understoodto date. One hypothesis proposes a viral etiology. Interestingly, viral proteins from humanendogenous retroviruses (HERVs) may play a role in the pathogenesis of MS. Allelic variants ofthe HERV-K18 env gene represent a genetic risk factor for MS, and the envelope protein is consideredto be an Epstein–Barr virus-trans-activated superantigen. To further specify a possible role forHERV-K18 in MS, the present study examined the immunogenicity of the purified surface unit (SU).HERV-K18(SU) induced envelope-specific plasma IgG in immunized mice and triggered proliferationof T cells isolated from these mice. It did not trigger phenotypic changes in a mouse model of experimentalautoimmune encephalomyelitis. Further studies are needed to investigate the underlyingmechanisms of HERV-K18 interaction with immune system regulators in more detail.