Bhatt P N, Jacoby R O
J Infect Dis. 1976 Aug;134(2):166-73. doi: 10.1093/infdis/134.2.166.
Genetic resistance of C3H/RV mice to lethal infection with Banzi virus (flavivirus) was severely compromised by immunosuppression with cyclophosphamide, sublethal X-irradiation, or thymus (T-) cell depletion. The mortality rate among immunosuppressed mice was usually 100%, but average survival times were shorter for mice treated with cyclophosphamide or for X-irradiated mice (10 days) than for T-cell-depleted mice (17 days). Mice treated with cyclophosphamide had high titers of virus in brain, lymphoid tissues, pancreas, and serum. Viral antigen was widespread in brain and pancreas, and mice developed nonsuppurative meningoencephalitis and pancreatitis. Yields of virus, spread of viral antigen, and lesions in T-cell-depleted mice were similar but less severe. Mice treated with cyclophosphamide did not have detectable hemagglutination-inhibiting antibody. T-cell-depleted mice developed hemagglutination-inhibiting antibody but were not protected from lethal infection. These results indicate that genetic resistance of C3H/RV mice to Banzi virus requires immunological factors, and that T-cells play a significant role in resistance to infection with Banzi virus.
环磷酰胺免疫抑制、亚致死剂量X射线照射或胸腺（T）细胞耗竭会严重损害C3H/RV小鼠对班齐病毒（黄病毒）致死性感染的遗传抗性。免疫抑制小鼠的死亡率通常为100%，但环磷酰胺处理的小鼠或X射线照射的小鼠（10天）的平均存活时间比T细胞耗竭的小鼠（17天）短。环磷酰胺处理的小鼠在脑、淋巴组织、胰腺和血清中具有高滴度的病毒。病毒抗原广泛存在于脑和胰腺中，小鼠发生非化脓性脑膜脑炎和胰腺炎。T细胞耗竭小鼠的病毒产量、病毒抗原传播和病变相似但较轻。环磷酰胺处理的小鼠没有可检测到的血凝抑制抗体。T细胞耗竭的小鼠产生了血凝抑制抗体，但未免受致死性感染。这些结果表明，C3H/RV小鼠对班齐病毒的遗传抗性需要免疫因素，并且T细胞在抵抗班齐病毒感染中起重要作用。
