Empig Cyril J, Goldsmith Mark A
Gladstone Institute of Virology and Immunology, San Francisco, California 94141-9100, USA.
J Virol. 2002 May;76(10):5266-70. doi: 10.1128/jvi.76.10.5266-5270.2002.
The filoviruses Ebola Zaire virus and Marburg virus are believed to infect target cells through endocytic vesicles, but the details of this pathway are unknown. We used a pseudotyping strategy to investigate the cell biology of filovirus entry. We observed that specific inhibitors of the caveola system, including cholesterol-sequestering drugs and phorbol esters, inhibited the entry of filovirus pseudotypes into human cells. We also measured slower cell entry kinetics for both filovirus pseudotypes than for pseudotypes of vesicular stomatitis virus (VSV), which has been recognized to exploit the clathrin-mediated entry pathway. Finally, visualization by immunofluorescence and confocal microscopy revealed that the filovirus pseudotypes colocalized with the caveola protein marker caveolin-1 but that VSV pseudotypes did not. Collectively, these results provide evidence suggesting that filoviruses use caveolae to gain entry into cells.
丝状病毒埃博拉-扎伊尔病毒和马尔堡病毒被认为是通过内吞小泡感染靶细胞的，但这一途径的具体细节尚不清楚。我们采用假型策略来研究丝状病毒进入细胞的细胞生物学。我们观察到，包括胆固醇螯合剂和佛波酯在内的小窝系统特异性抑制剂可抑制丝状病毒假型进入人类细胞。我们还测量了两种丝状病毒假型进入细胞的动力学比水泡性口炎病毒（VSV）假型更慢，VSV已被认为利用网格蛋白介导的进入途径。最后，通过免疫荧光和共聚焦显微镜观察发现，丝状病毒假型与小窝蛋白标记物小窝蛋白-1共定位，但VSV假型则不然。总的来说，这些结果提供了证据，表明丝状病毒利用小窝进入细胞。
