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首页> 外文期刊>Infection and immunity >Defense mechanisms against bovine herpesvirus: relationship of virus-host cell events to susceptibility to antibody-complement cell lysis.
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Defense mechanisms against bovine herpesvirus: relationship of virus-host cell events to susceptibility to antibody-complement cell lysis.

机译：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溶解敏感性的关系。

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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.
机译：检查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，以确定在病毒传播到易感邻近细胞之前或之后，体液免疫机制是否可以破坏被感染细胞。感染后6 h，在细胞膜上可检测到病毒抗原，但直到感染后10 h，细胞才对抗体补体裂解不敏感。在感染后10小时也可检测到细胞内感染性病毒，并从此时开始通过细胞内途径传播到相邻细胞。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，病毒的传播可以减少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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