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Human endogenous retrovirus-K18 Env as a risk factor in multiple sclerosisDepartment of Pathology, Tufts University School of Medicine, Boston, Massachusetts, USA
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, USA
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, USA
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts, USA aascheri{at}hsph.harvard.edu Background The human endogenous retrovirus (HERV)-K18 Env is an Epstein-Barr virus (EBV)-associated superantigen. Given the evidence for a role of EBV in the etiology of multiple sclerosis (MS), HERV-K18 Env is a plausible candidate for association with MS. Objective To assess whether variation in HERV-K18 Env is a risk factor for MS. Methods We developed a single nucleotide polymorphism-based genotyping method to determine the distribution of the three alleles of HERV-K18 env. We then conducted a nested case-control study including 207 MS cases and 403 matched controls. Analyses were replicated in an independent series of 909 MS cases and 339 controls. Results
Overall, there was a significant association between HERV-K18 env genotype and MS risk ( Conclusion Variation in EBV-associated superantigen HERV-K18 Env could influence the genetic susceptibility to MS.
Key Words: endogenous retroviruses • HERV-K18 • HLA • multiple sclerosis • polymorphisms
This version was published on November
1, 2008 Multiple Sclerosis, Vol. 14, No. 9,
1175-1180 (2008) |
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2 P = 0.03). As compared with K18.2/K18.2 individuals, risk of MS was three fold higher among K18.3/K18.3 individuals (P = 0.03). An increase in MS risk among carriers of the K18.3 allele was also observed in the replication study, but did not reach statistical significance. In pooled analyses, K18.3/K18.3 individuals had a significantly increased risk of MS (relative risks [RR] comparing K18.3/K18.3 vs K18.2/K18.2 = 2.7; 95% confidence interval: 1.1–6.4).