缺陷干扰流感病毒可抑制感染性病毒在小鼠体内的免疫病理效应。
Defective interfering influenza virus inhibits immunopathological effects of infectious virus in the mouse.
作者信息
Morgan D J, Dimmock N J
机构信息
Department of Biological Sciences, University of Warwick, Coventry, United Kingdom.
出版信息
J Virol. 1992 Feb;66(2):1188-92. doi: 10.1128/JVI.66.2.1188-1192.1992.
Abstract
Mice inoculated intranasally with a lethal dose of standard influenza virus die with an immune-mediated pneumonia but are protected by coinoculation with defective interfering (DI) virus. Here we show that recruitment of immune cells into the infected lung is halved by treatment with DI virus although the CD4+/CD8+ cell ratio is not affected. Responsiveness of lung T and B cells to lectins is inhibited by standard virus, but coinoculation of mice with DI virus causes a 13-fold increase in T-cell proliferation and up to a 100-fold increase in immunoglobulin production. This effect appears to be due to lymphocyte-specific DI virus-mediated interference, since there is no inhibition of virus multiplication in the lungs. The net result is a shift from a lethal to a beneficial immune response.
摘要
经鼻内接种致死剂量标准流感病毒的小鼠会因免疫介导的肺炎而死亡，但与缺陷干扰（DI）病毒共同接种可对其起到保护作用。我们在此表明，尽管CD4⁺/CD8⁺细胞比率未受影响，但用DI病毒处理后，进入受感染肺部的免疫细胞数量减半。标准病毒会抑制肺T细胞和B细胞对凝集素的反应性，但小鼠与DI病毒共同接种会使T细胞增殖增加13倍，免疫球蛋白产生增加多达100倍。这种效应似乎是由于淋巴细胞特异性DI病毒介导的干扰，因为肺部的病毒增殖未受抑制。最终结果是从致死性免疫反应转变为有益的免疫反应。
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