Brunet J P, Jourdan N, Cotte-Laffitte J, Linxe C, Géniteau-Legendre M, Servin A, Quéro A M
Institut National de la Santé et de la Recherche Médicale, Unité 510, Faculté de Pharmacie, Université Paris XI, 92296 Ch atenay-Malabry cedex, France.
J Virol. 2000 Nov;74(22):10801-6. doi: 10.1128/jvi.74.22.10801-10806.2000.
Rotavirus infection is the most common cause of severe infantile gastroenteritis worldwide. In vivo, rotavirus exhibits a marked tropism for the differentiated enterocytes of the intestinal epithelium. In vitro, differentiated and undifferentiated intestinal cells can be infected. We observed that rotavirus infection of the human intestinal epithelial Caco-2 cells induces cytoskeleton alterations as a function of cell differentiation. The vimentin network disorganization detected in undifferentiated Caco-2 cells was not found in fully differentiated cells. In contrast, differentiated Caco-2 cells presented Ca(2+)-dependent microtubule disassembly and Ca(2+)-independent cytokeratin 18 rearrangement, which both require viral replication. We propose that these structural alterations could represent the first manifestations of rotavirus-infected enterocyte injury leading to functional perturbations and then to diarrhea.
轮状病毒感染是全球范围内严重婴幼儿肠胃炎最常见的病因。在体内，轮状病毒对肠道上皮分化的肠细胞表现出明显的嗜性。在体外，分化和未分化的肠道细胞均可被感染。我们观察到，人肠道上皮Caco-2细胞感染轮状病毒会诱导细胞骨架改变，且这种改变是细胞分化的函数。在未分化的Caco-2细胞中检测到的波形蛋白网络紊乱在完全分化的细胞中未出现。相反，分化的Caco-2细胞呈现出Ca(2+)依赖的微管解聚和Ca(2+)非依赖的细胞角蛋白18重排，这两者均需要病毒复制。我们认为，这些结构改变可能代表轮状病毒感染的肠细胞损伤的最初表现，这种损伤会导致功能紊乱进而引发腹泻。
