Milton J D, Clements G B, Edwards R H
Department of Medicine, University of Liverpool, UK.
Postgrad Med J. 1991 Jun;67(788):532-7. doi: 10.1136/pgmj.67.788.532.
We have endeavoured to find immunological indications of chronic virus infection in patients with chronic fatigue syndrome (myalgic encephalomyelitis) and to investigate immune responsiveness to viruses in such patients in comparison with normal subjects and patients with muscular dystrophy. Levels of circulating IgM immune complexes were elevated (above the 95% normal control range) in 10 (17%) of 58 patients with chronic fatigue syndrome, which was not significantly different from the normal controls or from dystrophy controls (by Mann Whitney U test). Levels of IgG complexes were only increased in 10% of patients. Lymphocyte proliferation in response to concanavalin A (Con A), assessed by increase in 3H-thymidine incorporation, did not differ between 14 patients and 18 normal subjects. The proliferative response to Coxsackie B virus antigen did not differ between chronic fatigue patients and normal subjects when expressed either as an increase in counts or as a stimulation index. Adjustment of the counts in relation to the proliferation response to Con A, as an indication of the overall proliferative response of the cell preparation, did not reveal any hidden difference. IgM antibodies to Coxsackie B viruses were not found in any of 20 patients and in 1 of 20 dystrophy controls. Significant levels of neutralizing antibodies to Coxsackie B viruses 1-5 were found in 6 out of 19 (32%) patients compared with 4 out of 17 (24%) dystrophy controls, which does not differ from currently expected normal incidence. Antibody titres to other respiratory viruses were also not notably different between the patient and control groups. In conclusion we can find no evidence for a definable viral aetiology for the chronic fatigue syndrome, neither in terms of a persistent infection nor an altered ability to respond to virus.
我们致力于寻找慢性疲劳综合征（肌痛性脑脊髓炎）患者慢性病毒感染的免疫学指征，并与正常受试者及肌肉萎缩症患者相比，研究此类患者对病毒的免疫反应性。58例慢性疲劳综合征患者中有10例（17%）循环IgM免疫复合物水平升高（高于正常对照范围的95%），与正常对照组或肌肉萎缩症对照组相比无显著差异（通过曼-惠特尼U检验）。IgG复合物水平仅在10%的患者中升高。通过3H-胸腺嘧啶核苷掺入量增加评估的对刀豆球蛋白A（Con A）的淋巴细胞增殖，在14例患者和18例正常受试者之间无差异。慢性疲劳患者和正常受试者对柯萨奇B病毒抗原的增殖反应，无论是以计数增加还是刺激指数表示，均无差异。根据对Con A的增殖反应调整计数，作为细胞制剂总体增殖反应的指标，未发现任何隐藏差异。20例患者及20例肌肉萎缩症对照组中的1例均未发现针对柯萨奇B病毒的IgM抗体。19例患者中有6例（32%）发现针对柯萨奇B病毒1-5型的中和抗体水平显著，而17例肌肉萎缩症对照组中有4例（24%），这与目前预期的正常发生率无差异。患者组和对照组之间针对其他呼吸道病毒的抗体滴度也无明显差异。总之，我们找不到证据支持慢性疲劳综合征有明确的病毒病因，无论是持续性感染还是对病毒反应能力改变方面。
