Vaccinia virus K1L protein mediates host-range function in RK-13 cells via ankyrin repeat and may interact with a cellular GTPase-activating protein

被引:27
作者
Bradley, RR [1 ]
Terajima, M [1 ]
机构
[1] Univ Massachusetts, Sch Med, Ctr Infect Dis & Vaccine Res, Worcester, MA 01655 USA
关键词
D O I
10.1016/j.virusres.2005.06.003
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The K I L protein of vaccinia virus is required for its growth in certain cell lines (RK- 13 and human). The cowpox host-range protein CP77 has been shown to complement K I L function in RK- 13 Cells, despite a lack of homology between the two proteins except for ankyrin repeats. We investigated the role of ankyrin repeats of K I L protein in RK- 13 cells. The growth of a recombinant vaccinia virus, with KIL gene mutated in the most conserved ankyrin repeat, was severely impaired. Infection with the mutant virus caused shutdown of cellular and viral protein synthesis early in infection. We also investigated the interaction of K I L protein with cellular proteins and found that K I L interacts with the rabbit homologue of human ACAP2, a GTPase-activating protein with ankyrin repeats. Our result suggests the importance of ankyrin repeat for host-range function of KIL in RK-13 cells and identifies ACAP2 as a cellular protein, which may be interacting with KIL. (c) 2005 Elsevier B.V. All rights reserved.
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收藏
页码:104 / 112
页数:9
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