论文部分内容阅读
目的 :脊髓灰质炎 (脊灰 )病毒是引起脊髓灰质炎 (小儿麻痹 )的病原体。脊灰病毒 (PV)通过和敏感细胞表面的脊灰病毒受体 (PVR)结合而感染细胞。脊灰病毒感染后 ,细胞出现显著形态学改变 ,即细胞病变。本文的研究目的是探讨PV诱导的细胞病变机制。方法 :用PV野毒或光敏感株感染人神经细胞株(SK -N -SH) ,观察细胞病变发生的动态变化。同时用蚀斑实验和间接免疫荧光实验法检测病毒滴度和病毒抗原的分布。结果 :病毒感染 4小时后 ,细胞开始出现病变并释放子代病毒。感染后 4小时内 (即子代病毒释放前 )用抗PV或抗PVR单克隆抗体处理细胞则可以预防PV感染诱导的细胞病变。抗体处理前用野毒株再次攻击感染的细胞同样诱导细胞病变。相反 ,抗体处理前用光敏感病毒再次攻击感染的细胞后则减少细胞病变的发生。结论 :本研究结果显示 ,脊灰病毒引起的细胞病变由感染后产生的子代病毒的继发感染引起。
Purpose: Polio (polio) virus is the causative agent of poliomyelitis (poliomyelitis). Poliovirus (PV) infects cells by binding to the poliovirus receptor (PVR) on the surface of sensitive cells. After poliovirus infection, the cells showed significant morphological changes, namely cytopathic effect. The purpose of this study is to investigate the mechanism of PV-induced cytopathic effect. Methods: Human wild neuron cell line (SK -N -SH) was infected with wild-type or photosensitized PV and the dynamic changes of cytopathic effect were observed. At the same time, the virus titer and the distribution of virus antigens were detected by plaque test and indirect immunofluorescence test. Results: Four hours after virus infection, the cells started to develop lesions and release progeny virus. Treatment of cells with anti-PV or anti-PVR monoclonal antibodies within 4 hours after infection (ie, pre-progeny virus release) may prevent PV infection-induced cytopathic effects. Re-challenge of infected cells with wild-type strain prior to antibody treatment also induced cytopathic effect. In contrast, re-challenge of infected cells with light-sensitive virus prior to antibody treatment reduced the incidence of cytopathic effect. CONCLUSIONS: The results of this study show that the cytopathic effect caused by poliovirus is caused by the secondary infection of progeny virus produced after infection.