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针对牛疱疹病毒的防御机制:病毒-宿主细胞事件与抗体-补体细胞裂解易感性的关系

Defense mechanisms against bovine herpesvirus: relationship of virus-host cell events to susceptibility to antibody-complement cell lysis.

作者信息

Babiuk L A, Wardley R C, Rouse B T

出版信息

Infect Immun. 1975 Nov;12(5):958-63. doi: 10.1128/iai.12.5.958-963.1975.

Abstract

The interaction of infectious bovine rhinotracheitis virus and susceptible host cells was examined to determine whether an infected cell could be destroyed by humoral immune mechanisms before or after the transmission of virus to susceptible adjacent cells. Viral antigens were detectable on cell membranes at 6 h postinfection, but cells were not susceptible to antibody-complement lysis until 10 h postinfection. Intracellular infectious virus was also detectable at 10 h postinfection, and transmission to adjacent cells by the intracellular route began at this time. Extracellular virus was not detectable until 12 to 13 h postinfection. By the continual addition of antibody and complement, virus dissemination could be reduced more than 50-fold. These results support the hypothesis that the humoral immune mechanism may be involved in the recovery from herpesvirus infections.

摘要

研究了传染性牛鼻气管炎病毒与易感宿主细胞之间的相互作用,以确定受感染的细胞在病毒传播至易感相邻细胞之前或之后是否会被体液免疫机制破坏。感染后6小时可在细胞膜上检测到病毒抗原,但直到感染后10小时细胞才易被抗体-补体溶解。感染后10小时也可检测到细胞内感染性病毒,此时开始通过细胞内途径传播至相邻细胞。直到感染后12至13小时才检测到细胞外病毒。通过持续添加抗体和补体,病毒传播可减少50倍以上。这些结果支持体液免疫机制可能参与疱疹病毒感染恢复的假说。

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Immune mechanisms by which the spread of viral infections is stopped.阻止病毒感染传播的免疫机制。
Cell Immunol. 1974 Mar 30;11(1-3):478-83. doi: 10.1016/0008-8749(74)90045-8.

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