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阿根廷出血热。补体系统的改变及抗胡宁病毒体液反应。

Argentine hemorrhagic fever. Alterations of the complement system and anti-Junin-virus humoral response.

作者信息

de Bracco M M, Rimoldi M T, Cossio P M, Rabinovich A, Maiztegui J I, Carballal G, Arana R M

出版信息

N Engl J Med. 1978 Aug 3;299(5):216-21. doi: 10.1056/NEJM197808032990502.

Abstract

We investigated immunologic mechanisms and the role of complement in the pathogenesis of Argentine hemorrhagic fever, a disease caused by the Junin virus, a member of the arenavirus group. Total serum complement activity was reduced to 68 per cent of control values in patients with severe or moderate disease (P less than 0.001). C2, C3 and C5 values were also low (12 to 60 per cent) during the early acute period of the disease. However, serum C4 content was increased to 160 per cent of the control values in the same patients. Total complement activity returned to normal with clinical and laboratory recovery, at the time of detection of antibodies against Junin virus. C1q reactive material was found in four of 19 cases and no relation to the evolution of the disease could be established. These results suggest that immune complexes are not important in the pathogenesis of Argentine hemorrhagic fever, but that activation of the complement system has a role.

摘要

我们研究了免疫机制以及补体在阿根廷出血热发病机制中的作用。阿根廷出血热是由胡宁病毒引起的一种疾病,胡宁病毒属于沙粒病毒科。重症或中度患者的血清总补体活性降至对照值的68%(P<0.001)。在疾病的急性早期,C2、C3和C5值也较低(为对照值的12%至60%)。然而,同一批患者的血清C4含量增加至对照值的160%。随着临床和实验室指标的恢复,即检测到抗胡宁病毒抗体时,总补体活性恢复正常。19例患者中有4例检测到C1q反应性物质,但无法确定其与疾病进展的关系。这些结果表明,免疫复合物在阿根廷出血热的发病机制中并不重要,但补体系统的激活起到了一定作用。

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