Bipolar disorder (BD) is a chronic disease characterised by episodes of major depression and episodes of mania or hypomania, with a worldwide prevalence of 2.4%. The cause of BD is unknown. Here, I propose the hypothesis that BD is a chronic autoimmune disease caused by Epstein-Barr virus (EBV) infection of autoreactive B cells. It is postulated that EBV-infected autoreactive B cells accumulate in the brain where they provide costimulatory survival signals to autoreactive T cells and differentiate into plasma cells producing pathogenic autoantibodies targeting brain components such as the N-methyl-D-aspartate receptor. It is also proposed that the accumulation of EBV-infected autoreactive B cells in the brain is a consequence of a genetically determined defect in the ability of CD8+ T cells to control EBV infection. The theory is supported by studies indicating that autoimmunity, EBV infection and CD8+ T-cell deficiency all have roles in the pathogenesis of BD. According to the hypothesis, BD should be able to be treated by EBV-specific T-cell therapy and to be prevented by vaccination against EBV in early childhood. Exposure to sunlight or appropriate artificial light should also be beneficial in BD by augmenting CD8+ T-cell control of EBV infection.

中文翻译：

---

假设：躁郁症是一种由爱泼斯坦-巴尔病毒驱动的慢性自身免疫性疾病-对免疫疗法的影响。

躁郁症（BD）是一种慢性疾病，以严重抑郁发作和躁狂或轻躁狂发作为特征，全球患病率为2.4％。BD的原因尚不清楚。在这里，我提出一个假设，即BD是由自身反应性B细胞的爱泼斯坦-巴尔病毒（EBV）感染引起的慢性自身免疫性疾病。据推测，EBV感染的自身反应性B细胞在大脑中蓄积，在那里它们向自身反应性T细胞提供共刺激生存信号，并分化为浆细胞，产生针对大脑成分（例如N-甲基-D-天冬氨酸受体）的致病性自身抗体。也有人提出，EBV感染的自身反应性B细胞在大脑中的积累是CD8 + T细胞控制EBV感染的能力的遗传学决定的缺陷的结果。该理论得到了研究的支持，这些研究表明自身免疫性，EBV感染和CD8 + T细胞缺陷均与BD的发病机制有关。根据该假设，BD应该能够通过EBV特异性T细胞疗法进行治疗，并在儿童早期通过针对EBV的疫苗进行预防。通过增强CD8 + T细胞对EBV感染的控制，暴露于阳光或适当的人造光对BD也应是有益的。