Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Mult Scler. 2018 Jan;24(1):48-52. doi: 10.1177/1352458517737392.
Viruses have long been implicated as triggers of disease onset and progression in multiple sclerosis (MS) and similar neuroinflammatory disorders. Decades of epidemiological, molecular, and pathologic studies have most strongly linked the human herpesviruses Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) with MS. However, these viruses are ubiquitous in the general population and typically acquired decades before disease presentation, complicating the study of how they might contribute to disease. As experimental animal models may help elucidate mechanisms that have linked viruses with MS, we have been studying HHV-6 infections in a small nonhuman primate. We recently demonstrated that the subsequent induction of an MS-like experimental neuroinflammatory disease results in significantly accelerated disease in HHV-6 inoculated marmosets compared to controls. Ultimately, disease intervention in the form of clinical trials with an antiviral agent is the best way to concretely demonstrate a role for HHV-6 or any other virus in MS.
病毒长期以来一直被认为是多发性硬化症（MS）和类似神经炎症性疾病发病和进展的触发因素。数十年来的流行病学、分子和病理学研究最强烈地将人类疱疹病毒 EBV 和人类疱疹病毒 6（HHV-6）与 MS 联系在一起。然而，这些病毒在普通人群中普遍存在，通常在疾病发作前几十年就被感染，这使得研究它们如何导致疾病变得复杂。由于实验动物模型可能有助于阐明将病毒与 MS 联系起来的机制，我们一直在研究一种小型灵长类动物中的 HHV-6 感染。我们最近证明，随后诱导类似于 MS 的实验性神经炎症性疾病会导致 HHV-6 接种的狨猴的疾病明显加速，与对照组相比。最终，以抗病毒药物进行临床试验的疾病干预是具体证明 HHV-6 或任何其他病毒在 MS 中的作用的最佳方法。
