ACTIVATION OF THE ALTERNATIVE COMPLEMENT PATHWAY BY MUMPS INFECTED-CELLS - RELATIONSHIP TO VIRAL NEURAMINIDASE ACTIVITY
ACTIVATION OF THE ALTERNATIVE COMPLEMENT PATHWAY BY MUMPS INFECTED-CELLS - RELATIONSHIP TO VIRAL NEURAMINIDASE ACTIVITY
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DOI：
10.1007/bf01315298
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发表时间：
1986-01-01
影响因子：
2.7
通讯作者：
WINKELSTEIN, JA
中科院分区：
文献类型：
--
作者：
HIRSCH, RL;WOLINSKY, JS;WINKELSTEIN, JA
颗粒的唾液酸含量与其激活补体旁路途径的能力之间存在反比关系。本研究旨在确定不同腮腺炎病毒株的神经氨酸酶（NANase）活性是否会影响腮腺炎病毒感染细胞激活旁路途径的能力。用三种不同的腮腺炎病毒株（RW、O“Take和Kilham）感染CV-1细胞，24小时后，将用EGTA/MgCl 2处理的10%豚鼠血清（GPS）或缺乏补体第四组分的GPS（C4DGPS）加入细胞单层。30分钟后，通过功能性溶血试验测定消耗的C3百分比。感染RW（高NANase）的细胞消耗的C3（23.2%）明显多于Kilham（5.7%，低NANase）。感染O '' Take的细胞激活C3的能力中等。通过荧光显微镜检测，感染细胞表面的C3沉积程度也大于感染RW的细胞，而不是Kilham腮腺炎病毒株。这些研究表明，腮腺炎病毒的NANase活性可以影响感染细胞激活旁路途径的能力，从而影响补体参与宿主防御腮腺炎病毒感染的能力。
An inverse relationship exists between the sialic acid content of a particle and its ability to activate the alternative complement pathway. The present studies were performed to determine if the neuraminidase (NANase) activities of different mumps virus strains could influence the ability of mumps virus infected cells to activate the alternative pathway. CV-1 cells were infected with three different mumps virus strains (RW, O''Take, and Kilham) and after 24 hours, 10 percent guinea pig serum (GPS) treated with EGTA/MgCl2 or GPS lacking the 4th component of complement (C4DGPS) was added to the cell monolayers. After 30 minutes, th percentage C3 consumed was determined by a functional hemolytic assay. Cells infected with RW (high NANase) consumed significantly more C3 (23.2 per cent) than cells infected with Kilham (5.7 percent, low NANase). Cells infected with O''Take were intermediate in their ability to acitvate C3. The degree of C3 deposition on the surface of infected cells, detected by fluorescence microscopy, was also greater for cells infected with the RW than the Kilham strain of mumps virus. These studies suggest that the NANase activity of mumps virus can influence the ability of infected cells to activate the alternative pathway and thereby, the ability of complement to participate in host defense against mumps virus infection.