期刊
MULTIPLE SCLEROSIS JOURNAL
卷 15, 期 4, 页码 431-436出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/1352458508100037
关键词
epidemiology; HLA-DRB1*15; immunology; infectious mononucleosis; multiple sclerosis
资金
- Danish Research Council
- Dagmar Marshall Foundation
- The Pharmaceutical foundation
- Foundation of Civil engineer Bent Bogh and wife Inge Bogh
- Director Ejnar Jonasson
- Johnsen and Wife's Memorial Foundation
- Gangsted Foundation
- Danish Multiple Sclerosis Society
- Foundation of Aase and Ejnar Danielsen
- Obelske family foundation
Background Both human leukocyte antigen (HLA)-DRB1*15 and Epstein-Barr virus infection presenting as infectious mononucleosis (IM) are recognized as risk factors for multiple sclerosis (MS). However, their combined effect and possible interaction on MS risk is not known. Objective To assess the association between HLA-DRB1*15 and risk of MS in persons with and without IM. Methods We compared the prevalence of DRB1*15 in MS patients with (n = 76) and without (n = 1,836) IM with the corresponding distributions in blood donors with (n = 62) and without (n = 484) IM histories. This allowed us to estimate the relative risk of MS associated with DRB1*15 in the presence and absence, respectively, of previous IM. We then estimated the interaction between DRB1*15 and IM as the ratio of the two individual odds ratios. Results In IM-naive individuals, DRB1*15 carried a 2.4-fold (95% confidence interval [CI], 2.0-3.0) increased MS risk. In contrast, among persons with IM history, DRB1*15 was associated with a 7.0-fold (95% CI, 3.3-15.4) increased MS risk. Thus, the MS risk conferred by HLA-DRB1*15 was 2.9 (95% CI, 1.3-6.5)-fold stronger in the presence than in the absence of IM. Combined with previous results, this result indicates that DRB1*15-positive persons with a history of IM may be at a 10.0-fold (95% CI, 6.0-17.9) increased risk of MS compared with persons who are DRB1*15 and IM-naive. Conclusion DRB1*15 and IM may act in synergy causing MS. Multiple Sclerosis 2009; 15: 431-436. http://msj.sagepub.com
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