Med Hypotheses. 2009 Nov;73(5):728-34. doi: 10.1016/j.mehy.2009.04.043. Epub 2009 Jun 10.
This article posits that infection of the peripheral ganglia causes at least some cases of Chronic Fatigue Syndrome (CFS), with a neurotropic herpesvirus, particularly varicella-zoster virus (VZV), as the most likely cause of the infection. Virtually all CFS symptoms could be produced by an infection of the peripheral ganglia, with infection of the autonomic ganglia causing fatigue, postural hypotension, and sleep disturbances, and infection of the sensory ganglia causing sensory symptoms such as chronic pain. Furthermore, infections of the peripheral ganglia are known to cause long-term nerve dysfunction, which would help explain the chronic course of CFS. Herpesviruses have long been suspected as the cause of CFS; this theory has recently been supported by studies showing that administering antiherpes agents causes substantial improvement in some CFS patients. VZV is known to frequently reactivate in the peripheral ganglia of previously healthy adults and cause sudden, debilitating illness, making it a likely candidate as a cause of CFS. Moreover, many of the symptoms of CFS overlap with those of herpes zoster (shingles), with the exception that painful rash is not one of the symptoms of CFS. A model is therefore proposed in which CFS is one of the many manifestations of zoster sine herpete; that is, herpes zoster without rash. Furthermore, re-exposure to VZV in the form of chickenpox has become less common in the past few decades; without such re-exposure, immunity to VZV drops, which could explain the increased incidence of CFS. Co-infection with multiple herpesviruses is a possibility, as some CFS patients show signs of infection with other herpesviruses including Epstein-Barr, Cytomegalovirus, and HHV6. These three herpesviruses can attack immune cells, and may therefore promote neurotropic herpesvirus reactivation in the ganglia. The possibility of VZV as the causal agent in CFS has previously received almost no attention; the possibility that CFS involves infection of the peripheral ganglia has likewise been largely overlooked. This suggests that the search for a viral cause of CFS has been far from exhaustive. Several antiherpes drugs are available, as is a vaccine for VZV; more research into such agents as possible treatments for CFS is urgently needed.
本文提出，外周神经节感染至少是慢性疲劳综合征（CFS）的部分病因，其中神经亲和性疱疹病毒，尤其是水痘带状疱疹病毒（VZV），是最有可能的感染源。几乎所有 CFS 症状都可能由外周神经节感染引起，自主神经节感染导致疲劳、体位性低血压和睡眠障碍，而感觉神经节感染导致慢性疼痛等感觉症状。此外，外周神经节感染已知会导致长期神经功能障碍，这有助于解释 CFS 的慢性病程。疱疹病毒一直被怀疑是 CFS 的病因；最近的研究支持了这一理论，该研究表明，给予抗疱疹药物可使部分 CFS 患者的病情显著改善。VZV 已知在以前健康的成年人的外周神经节中频繁重新激活，并导致突然的衰弱性疾病，使其成为 CFS 病因的一个可能候选者。此外，CFS 的许多症状与带状疱疹（带状疱疹）重叠，除了疼痛皮疹不是 CFS 的症状之一。因此，提出了一种模型，即 CFS 是无皮疹带状疱疹的多种表现形式之一；也就是说，无皮疹的带状疱疹。此外，过去几十年中，水痘形式的 VZV 再次暴露变得不那么常见；没有这种再次暴露，VZV 的免疫力下降，这可以解释 CFS 发病率的增加。多种疱疹病毒的合并感染是一种可能性，因为一些 CFS 患者表现出感染其他疱疹病毒的迹象，包括 EBV、巨细胞病毒和 HHV6。这三种疱疹病毒可以攻击免疫细胞，因此可能促进神经亲和性疱疹病毒在神经节中的重新激活。VZV 作为 CFS 致病因子的可能性以前几乎没有受到关注；CFS 涉及外周神经节感染的可能性也在很大程度上被忽视。这表明，寻找 CFS 的病毒病因还远远不够全面。有几种抗疱疹药物和 VZV 疫苗可用；迫切需要更多研究这些药物作为 CFS 可能的治疗方法。
