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Effect of immunosuppression on the genetic resistance of A2G mice to neurovirulent influenza virus.

机译:免疫抑制对A2G小鼠对神经毒性流感病毒的遗传抗性的影响。

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A2G mice are genetically resistant to lethal infection with neurotropic and pneumotropic influenza viruses. A possible immunological explanation for this resistance was sought by assessing the effect of cyclophosphamide and X irradiation immunosuppression on the infection of A2G mice with lethal doses of neurovirulent virus. Immunosuppressed A2G mice survived lethal infection enen though rendered unable to produce specific antiviral antibody or to generate cell-mediated delayed-type hypersensitivity responses. Measurement of infectious virus replication and detailed observation of the infection by immunofluorescence microscopy show that immunosuppression does not potentiate or allow spread of the virus in A2G brains. Interferon levels were essentially the same in normal and immunosuppressed A2G brains but were 3 to 5 times lower than in the brains of susceptible mice dying of the infection. The results strongly suggest that the genetic resistance of A2G mice to the acute lethal effects of neurovirulent influenza virus infection does not depend on the induction of primary immune mechanisms as we currently understand them. Other possible explanations for this resistance are considered.
机译:A2G小鼠在遗传上抵抗嗜神经性和嗜肺性流感病毒的致死性感染。通过评估环磷酰胺和X射线免疫抑制对致死剂量的神经毒性病毒A2G小鼠感染的影响,寻求了对此耐药性的可能的免疫学解释。免疫抑制的A2G小鼠虽然无法产生特异性抗病毒抗体或无法产生细胞介导的迟发型超敏反应,但仍能承受致命的感染。感染性病毒复制的测量和通过免疫荧光显微镜对感染的详细观察表明,免疫抑制不会增强病毒或不允许病毒在A2G大脑中传播。正常和免疫抑制的A2G大脑中的干扰素水平基本相同,但比死于感染的易感小鼠的大脑中的干扰素水平低3至5倍。结果强烈表明,A2G小鼠对神经毒力流感病毒感染的急性致死作用的遗传抗性不依赖于目前我们了解的主要免疫机制的诱导。考虑对该阻力的其他可能解释。

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