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目的比较柯萨奇病毒B组3型(coxsackievirus B3,CV-B3)和肠道病毒71型(enterovirus 71,EV-A71)的入胞机制。方法分别用CV-B3和EV-A71感染经不同小分子入胞抑制剂处理后的HeLa细胞,通过细胞免疫染色及图像分析,量化比较感染结果。结果细胞松弛素D、长春碱、巴弗洛霉素A1及布雷菲德菌素A均能抑制CV-B3和EV-A71对HeLa细胞的早期感染,表明两种病毒的入胞过程均需要细胞骨架、内吞小体酸化及膜泡运输作用;肝素能抑制EV-A71的感染并呈浓度依赖关系,但对CV-B3无显著作用,表明细胞膜表面的硫酸乙酰肝素参与EV-A71但可能不参与CV-B3的入胞过程;巴弗洛霉素A1对EV-A71的抑制更明显,说明在病毒脱衣壳过程中,EV-A71较CV-B3依赖更低的pH;细胞骨架抑制剂处理结果表明CV-B3的入胞过程更依赖于微管蛋白而非微丝蛋白的作用。结论 CV-B3和EV-A71具有相似的入胞机制,但却各具特点,为研究两者的抗病毒药物提供了依据。
Objective To compare the mechanism of entry of coxsackievirus B3 (CV-B3) and enterovirus 71 (EV-A71). Methods HeLa cells treated with different small molecule inhibitors were infected with CV-B3 and EV-A71, respectively. The results of infection were quantified by immunocytochemistry and image analysis. Results Cytochalasin D, vinblastine, bafilomycin A1 and brefeldin A all inhibited the early infection of HeLa cells by CV-B3 and EV-A71, indicating that both viruses require cells Heparin inhibits the infection of EV-A71 in a concentration-dependent manner, but has no significant effect on CV-B3, indicating that heparan sulfate on the cell membrane may participate in EV-A71 but may not Which is involved in the entry of CV-B3. The inhibition of EV-A71 by bafilomycin A1 is more obvious, indicating that EV-A71 relies on a lower pH than CV-B3 during virus shedding. Cytoskeleton inhibitor treatment The results indicate that the entry of CV-B3 is more dependent on tubulin than on fibroin. Conclusions CV-B3 and EV-A71 have similar mechanism of cell entry, but they have their own characteristics and provide the basis for the study of both antiviral drugs.