Slusarczyk J, Hansson B G, Nordenfelt E, Krawczyński K, Karwowska S, Knap J
J Med Virol. 1984;14(3):269-76. doi: 10.1002/jmv.1890140311.
The anti-HAV humoral immune response in the IgM, IgA, and IgG classes was analyzed weekly in 35 patients with clinically overt hepatitis A during the time of their hospitalization and 2-3 years afterward. In parallel, the dynamics of total immunoglobulins and complement C3 component (C3) levels were determined. The results suggest that the appearance of class-specific anti-HAV is compatible with the course of primary humoral immune response, with IgM and IgA anti-HAV, providing immunity in the early and intermediate phases of the infection, and IgG anti-HAV, providing immunity in the later phase. The overall appearance of anti-HAV, total immunoglobulins, and C3, do not support the view that liver injury is mediated by the humoral immune mechanisms. Instead, the hepatocyte damage is probably caused by direct viral cytotoxicity. This hypothesis is supported by a case of hepatitis A in a patient under immunosuppressive treatment.
在35例临床显性甲型肝炎患者住院期间及之后的2至3年里，每周分析其IgM、IgA和IgG类抗甲型肝炎病毒（anti-HAV）体液免疫反应。同时，测定总免疫球蛋白和补体C3成分（C3）水平的动态变化。结果表明，特异性抗-HAV类别的出现与原发性体液免疫反应过程相符，IgM和IgA抗-HAV在感染的早期和中期提供免疫，而IgG抗-HAV在后期提供免疫。抗-HAV、总免疫球蛋白和C3的总体表现不支持肝损伤由体液免疫机制介导的观点。相反，肝细胞损伤可能是由直接病毒细胞毒性引起的。免疫抑制治疗患者的一例甲型肝炎病例支持了这一假说。
