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The Etiology of Multiple Sclerosis: Genetic Evidence for the Involvement of the Human Endogenous Retrovirus HERV-Fc1

机译:多发性硬化症的病因:人类内源性逆转录病毒HERV-Fc1参与的遗传证据。

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We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis.
机译:我们通过分析4个队列中患者和对照的DNA来研究人类内源性逆转录病毒在多发性硬化中的作用,以研究多发性硬化症与病毒限制性基因或具有一个或多个完整或几乎完整基因的内源性逆转录病毒基因座附近的多态性之间的关联。我们发现基因TRIM5中的SNP与疾病呈负相关。相反,一个逆转录病毒基因座HERV-Fc1周围的SNPs与疾病高度相关。后者的关联仅限于不包含其他已知基因的狭窄区域。我们得出结论,HERV-Fc1和TRIM5在多发性硬化的病因中起作用。如果这些结果得到证实,则表明了多发性硬化症的新治疗方式。

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