Newcastle disease virus may enter cells by caveolae-mediated endocytosis
Newcastle disease virus may enter cells by caveolae-mediated endocytosis
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DOI：
10.1099/vir.0.82150-0
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发表时间：
2007-02-01
影响因子：
3.8
通讯作者：
Munoz-Barroso, Isabel
中科院分区：
文献类型：
--
作者：
Cantin, Celia;Holguera, Javier;Munoz-Barroso, Isabel
新城疫病毒(NDV)是副粘病毒的原型成员，其进入细胞的机制被认为是通过与pH无关的机制在质膜上直接融合而发生的。此外，新城疫病毒可能通过内吞途径进入宿主细胞。用阻断小窝依赖的内吞作用的药物处理细胞会降低新城疫病毒的融合率和传染性，抑制程度取决于病毒浓度。病毒吸附后再加药，抑制作用大大减弱。用甲基β-环糊精(一种将胆固醇从细胞膜中隔离出来的药物)处理的细胞，降低了融合程度、传染性和病毒与细胞的结合；这表明胆固醇在新城疫病毒进入过程中发挥了作用。用抗新城疫病毒的单抗和针对早期内体标记EEA1的抗体进行的双标记LING免疫荧光分析显示病毒在这些细胞内结构中的定位。荧光显微镜观察发现，在低pH条件下，细胞-细胞融合增强。结论新城疫病毒可能通过小窝依赖的内吞途径感染细胞，提示该途径可能是病毒进入细胞的另一种途径。
The entry into cells of Newcastle disease virus (NDV), a prototype member of the paramyxoviruses, is believed to occur by direct fusion at the plasma membrane through a pH-independent mechanism. In addition, NDV may enter host cells by an endocytic pathway. Treatment of cells with drugs that block caveolae-dependent endocytosis reduced NDV fusion and infectivity, the degree of inhibition being dependent on virus concentration. The inhibitory effect was reduced greatly when drugs were added after virus adsorption. Cells treated with methyl beta-cyclodextrin, a drug that sequesters cholesterol from membranes, reduced the extent of fusion, infectivity and virus-cell binding; this indicates that cholesterol plays a role in NDV entry. Double-label ling immunofluorescence assays performed with anti-NDV monoclonal antibodies and antibodies against the early endosome marker EEA1 revealed the localization of the virus in these intracellular structures. Using fluorescence microscopy, it was found that cell-cell fusion was enhanced at low pH. It is concluded that NDV may infect cells through a caveolae-dependent endocytic pathway, suggesting that this pathway could be an alternative route for virus entry into cells.