白细胞介素-1β缺陷小鼠对致命性辛德毕斯病毒脑炎的抗性。
Resistance of interleukin-1beta-deficient mice to fatal Sindbis virus encephalitis.
作者信息
Liang X H, Goldman J E, Jiang H H, Levine B
机构信息
Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA.
出版信息
J Virol. 1999 Mar;73(3):2563-7. doi: 10.1128/JVI.73.3.2563-2567.1999.
Interleukin-1beta (IL-1beta) concentrations are frequently elevated in central nervous system (CNS) viral infections, but the pathophysiologic significance of such elevations is not known. To examine the role of IL-1beta in CNS viral pathogenesis, we compared the natural histories of IL-1beta-deficient and wild-type 129 SV(ev) mice infected with a neurovirulent viral strain, neuroadapted Sindbis virus (NSV). We found that the incidence of severe paralysis and death was markedly decreased in NSV-infected IL-1beta-/- mice compared to NSV-infected wild-type mice (4 versus 88%, P < 0.001). Despite this marked difference in clinical outcome, no differences in numbers of apoptotic cells or presence of histopathologic lesions in the brains of moribund wild-type mice and those of clinically healthy IL-1beta-/- mice could be detected. These results suggest that IL-1beta deficiency is protective against fatal Sindbis virus infection by a mechanism that does not involve resistance to CNS virus-induced apoptosis or histopathology.
白细胞介素-1β（IL-1β）浓度在中枢神经系统（CNS）病毒感染中常升高，但其升高的病理生理意义尚不清楚。为研究IL-1β在CNS病毒发病机制中的作用，我们比较了感染神经毒力病毒株——神经适应性辛德毕斯病毒（NSV）的IL-1β缺陷型和野生型129 SV(ev)小鼠的自然病程。我们发现，与感染NSV的野生型小鼠相比，感染NSV的IL-1β基因敲除小鼠严重麻痹和死亡的发生率显著降低（4%对88%，P<0.001）。尽管临床结果存在显著差异，但濒死野生型小鼠和临床健康的IL-1β基因敲除小鼠大脑中的凋亡细胞数量或组织病理学损伤情况均未检测到差异。这些结果表明，IL-1β缺陷通过一种不涉及对CNS病毒诱导的凋亡或组织病理学产生抗性的机制，对致命的辛德毕斯病毒感染具有保护作用。
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