Konno T, Suzuki H, Kitaoka S, Sato T, Fukuhara N, Yoshie O, Fukudome K, Numazaki Y
Department of Pediatrics, Medical School Tohoku University, Sendai, Japan.
Clin Infect Dis. 1993 Mar;16 Suppl 2:S92-7. doi: 10.1093/clinids/16.supplement_2.s92.
Rotaviruses are the most important etiologic agents of severe diarrhea worldwide. Despite great advances in vaccine development, little is known about host protection mechanisms other than immunity. This presentation focuses on the proteolytic enhancement of rotavirus infection, with emphasis on the functions of VP4, an outer capsid protein. The in vitro growth of human rotavirus is enhanced by trypsin, which selectively cleaves VP4. Treatment with trypsin increases the infectivity of human rotavirus while decreasing its hemagglutination activity. There are two modes of rotavirus internalization: direct penetration with the aid of trypsin and endocytosis without trypsin. Direct penetration via VP4 cleaved by trypsin is essential for the replication of the virus, whereas endocytotic internalization does not give rise to viral replication.
轮状病毒是全球范围内严重腹泻的最重要病因。尽管疫苗研发取得了巨大进展,但除免疫之外,人们对宿主保护机制知之甚少。本报告重点关注轮状病毒感染的蛋白水解增强作用,尤其强调外衣壳蛋白VP4的功能。人轮状病毒的体外生长可被胰蛋白酶增强,胰蛋白酶可选择性切割VP4。用胰蛋白酶处理可增加人轮状病毒的感染性,同时降低其血凝活性。轮状病毒有两种内化模式:借助胰蛋白酶的直接穿透和不借助胰蛋白酶的内吞作用。经胰蛋白酶切割的VP4介导的直接穿透对于病毒复制至关重要,而内吞内化则不会引发病毒复制。