Marsh M, Bron R
MRC Laboratory for Molecular Cell Biology, University College London, UK.
J Cell Sci. 1997 Jan;110 ( Pt 1):95-103. doi: 10.1242/jcs.110.1.95.
Alphaviruses, such as Semliki Forest virus, normally enter cells by penetration from acidic organelles of the endocytic pathway. The virions are internalised intact from the cell surface before undergoing acid-induced fusion in endosomes. To investigate the possibility that endocytosis might play a role in delivering virions to specific sites for replication, we compared SFV infection of baby hamster kidney (BHK) cells and Chinese hamster ovary (CHO) cells following either normal virus fusion in endosomes or experimentally-induced fusion at the cell surface. Whereas baby hamster kidney cells were infected efficiently following fusion in endosomes or at the plasma membrane, Chinese hamster ovary cells were only infected following fusion from endocytic organelles. Virions fused at the plasma membrane of CHO cells failed to initiate viral RNA and protein synthesis. Similar results were observed when CHO cells were challenged with a rhabdovirus, vesicular stomatitis virus. These data suggest that in certain cell types a barrier, other than the plasma membrane, can prevent infection by alpha- and rhabdoviruses fused at the cell surface. Moreover, they suggest the endocytic pathway provides a mechanism for bringing viral particles to a site, or sites, in the cell where replication can proceed.
甲病毒，如Semliki森林病毒，通常通过从内吞途径的酸性细胞器穿透进入细胞。病毒粒子在细胞表面完整内化，然后在内体中发生酸诱导融合。为了研究内吞作用是否可能在将病毒粒子递送至特定复制位点中发挥作用，我们比较了在正常内体病毒融合或实验诱导的细胞表面融合后，婴儿仓鼠肾（BHK）细胞和中国仓鼠卵巢（CHO）细胞对Semliki森林病毒（SFV）的感染情况。虽然婴儿仓鼠肾细胞在内体或质膜融合后能有效感染，但中国仓鼠卵巢细胞仅在从内吞细胞器融合后才被感染。在CHO细胞质膜融合的病毒粒子未能启动病毒RNA和蛋白质合成。当用弹状病毒水疱性口炎病毒攻击CHO细胞时，也观察到了类似结果。这些数据表明，在某些细胞类型中，除质膜外的一种屏障可阻止在细胞表面融合的甲病毒和弹状病毒感染。此外，它们表明内吞途径提供了一种机制，可将病毒颗粒带到细胞内一个或多个复制可以进行的位点。
