摘要
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。
Objective: Poliovirus is the etiologic agent of poliomyelitis. The initial event of poliovirus infection is the attachment of the virion to poliovirus receptor (PVR), which is found only on the surfaces of primate cells. The productive infection of permissive cells with poliovirus induces dramatic morphological alterations termed cytopathic effect. Methods: Human neuroblastoma cells (SK-N-SH) infected with type I poliovirus Mahoney strain (PV1/Mahoney) displayed typical signs of CPE at 4 hours post-infection. Analysis of the kinetics of virus production from PV1/Mahoney-infected SK-N-SH cells demonstrated that the newly synthesized viruses appeared at 4 hours post-infection. Results: Treatment with specific antibodies against PV1/Mahoney or PVR within 4 hours post-infection protected most of the infected cells from development of cytopathic effect. Before addition of antibodies, re-infection of the infected cells with wild type viruses induced CPE and cell death. However, before antibody treatment re-infection of the infected cells with the inac-tivated polioviruses significantly reduced virus-induced cytopathic effect. Conclusion: Our results suggested that secondary infection of the cells was critical to the development of PV-induced cytopathic effect.
出处
《河南医学研究》
CAS
2004年第2期97-102,共6页
Henan Medical Research
