Syncytin, a protein encoded by a human endogenous retrovirus (HERV) envelop gene, is associated with redoxrelated death of oligodendrocytes and demyelination in lesions in the brains of patients with multiple sclerosis (MS). HERVs are sections of the human genome that originated as retroviral DNA transcripts and became integrated into human chromosomes. Chris Power (University of Calgary, Canada), lead author of the paper explained that, although most of the 20 or so different families of HERVs scattered around the human genome are quiescent, several HERVs have been implicated in physiological processes and disease. Power and colleagues in Canada, France, the UK, and the USA examined the abundance of different HERV mRNAs in the brains of patients with MS. After finding an abundance of HERV-W env mRNA, the researchers used western blotting to look for syncytin, the protein encoded by this gene. Patients with MS had three times the amount of syncytin found in the brains of healthy people (Nat Neurosci

2004; 7: 1088–95). Moreover, syncytin was selectively expressed in astrocytes and microglia—cells that mediate neuroinflammation. When the researchers investigated the effects of syncytin in human fetal astrocytes, they found release of reactive oxygen species and subsequent upregulation of proinflammatory molecules in glia. Power and colleagues also found that soluble factors released by astrocytes in response to syncytin led to oligodendrocyte damage death.“We are the first group to show that an HERV envelope protein has the ability to be pathogenetic”, says Power.“HERV-W is no longer just a virus you can find expressed in patients with MS without any knowledge of its significance”, says Anné Møller-Larsen (Institute of Medical Microbiology and Immunology, University of Aarhus, Denmark).“Now it has been shown that it can be at least part of the cause of the pathological findings in patients with MS.” Power, however, does not think syncytin is the cause of MS, although “it certainly could be an