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Epstein-Barr virus infection in multiple sclerosis and control subjects: an HLA association study

Epstein-Barr virus infection in multiple sclerosis and control subjects: an HLA association study
多发性硬化症和对照受试者中的 Epstein-Barr 病毒感染:一项 HLA 关联研究
批准号:
G0801975/1
负责人:
Gavin Giovannoni
金额:
$61.7万
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2009
资助国家:
英国
项目状态:
已结题
起止时间:
2009 至 --

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中文摘要
翻译
虽然多发性硬化症被认为是一种自身免疫性疾病,其中身体?由于多发性硬化症患者自身的免疫系统攻击中枢神经系统(CNS)的髓鞘,因此尚未明确排除多发性硬化症的特定感染原因。几项研究已经证明了引起腺热和多发性硬化的病毒之间的联系。这种病毒被称为爱泼斯坦-巴尔病毒(EBV),它是疱疹病毒群的一员。像其他疱疹病毒一样,eb病毒有能力潜伏在体内,并间歇性地重新激活自己。这些EBV再激活的发作通常不会引起症状,但在多发性硬化症患者中,它们可能引发临床发作。几乎所有多发性硬化症患者都感染了EBV,而在普通人群中,这一比例仅为90%。虽然这种差异可能看起来很小,但它非常重要,并且是许多研究中一致的发现。由于最初感染eb病毒而出现症状(即感染性单核细胞增多症,通常称为腺热)的人与最初感染eb病毒而没有症状的人相比,将来发展为MS的风险更高。研究免疫系统的科学家已经证明,具有攻击髓磷脂潜力的白细胞也可以被EBV激活。与正常对照者相比,多发性硬化症患者的血液中有EBV持续或近期再激活的证据。最近有一项研究表明,多发性硬化症患者EBV的再激活与多发性硬化症发作或复发密切相关。总的来说,上述证据表明EBV感染和EBV感染的间歇性再激活与MS疾病活动有关。我们想研究:(1)患有多发性硬化症的兄弟姐妹,看看有无多发性硬化症的兄弟姐妹在EBV感染率方面是否存在差异;(2)健康对照,观察是否由于缺乏易感基因而保持EBV阴性并对多发性硬化症有抵抗力的人;(3)确定患有多发性硬化的成年人是否更容易携带与MS相关的基因;(4)确定多发性硬化症患者是否更容易携带已被证明易患腺热或传染性单核细胞增多症的基因。
英文摘要
Although MS is believed to be an autoimmune disease in which the body?s own immune system attacks the myelin sheaths in the central nervous system (CNS), a specific infectious cause for MS has not been definitively excluded. Several studies have demonstrated a link between the virus which causes glandular fever and MS. This virus is called Epstein-Barr Virus (EBV), which is a member of the herpes group of viruses. EBV, like the other herpes viruses, has the ability to lie dormant or latent in the body and to reactivate itself intermittently. These episodes of EBV reactivation generally do not cause symptoms, but in people with MS they may trigger clinical attacks. Almost all people with MS are infected with EBV compared to only 9 out of 10 people in the general population. Although this difference may seem small it is highly significant and a consistent finding across numerous studies. People who have symptoms (i.e. infectious mononucleosis, often called glandular fever) as a result of their initial EBV infection have an increased risk of developing MS in the future compared to people who do not experience symptoms with their initial EBV infection. Scientists who study the immune system have demonstrated that white blood cells with the potential to attack myelin can also be activated by EBV. People with MS have evidence of ongoing or recent reactivation of EBV in their blood compared to normal control subjects. More recently there has been a study demonstrating that reactivation of EBV in people with MS is closely linked to onset of MS attacks or relapses. Overall, the above evidence suggests that EBV infection and the intermittent reactivation of EBV infection are linked to MS disease activity. We want to study: (1) sibling pairs with MS to see if there are any differences between sibling pairs with and without MS in relation to the rate of EBV infection; (2) healthy controls to see if people who remain EBV negative and are resistant to developing MS because they lack genes that make them susceptible to developing MS; (3) establish whether or not adults who develop IM are more likely to carry genes associated with MS; (4) establish whether or not people with MS are more likely to be carry genes, which have been shown to predispose to glandular fever or infectious mononucleosis.
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