請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/71171
標題: Restriction of vaccinia virus replication by a ced-3 and ced-4-dependent pathway in Caenorhabditis elegans
作者: Liu, W.H.
Lin, Y.L.
Wang, J.P.
Liou, W.
Hou, R.F.
Wu, Y.C.
Liao, C.L.
關鍵字: programmed cell death
virus-host interaction
programmed cell-death
nematode c-elegans
innate immunity
interleukin-1-beta-converting enzyme
microbial virulence
gene ced-3
protein
model
apoptosis
pathogenesis
期刊/報告no:: Proceedings of the National Academy of Sciences of the United States of America, Volume 103, Issue 11, Page(s) 4174-4179.
摘要: Genetic tractability and easy manipulation make Caenorhabditis elegans a good model to study host-pathogen interactions. Dozens of different bacterial species can pathogenically infect C elegans under laboratory conditions, and all of these microbes are extracellular pathogens to nematodes. Viruses, on the other hand, are obligate intracellular parasites, and yet no viral infections have been reported for C elegans. We established a procedure allowing vaccinia virus to enter and subsequently replicate in C elegans. Virus replication was significantly enhanced in ced-3, ced-4, ced9(gf), and egl-1(If) mutants, demonstrating that the core programmed cell death (PCD) genes ced-3, ced-4, ced-9, and egl-1 control vaccinia virus replication in C elegans. The ability of ced-3 and ced-4 alleles to restrict virus replication is correlated with their cell-killing activities. Moreover, the increase in vaccinia virus replication levels in the PCD-defective mutants was not likely to be caused by the extra live cells, as neither the inhibition of PCD by icd-1 overexpression nor the presence of extra cells after extra cell divisions in cul-1 or lin-23 mutants had any significant effect on vaccinia virus replication. Therefore, the core PCD genes possess a unique function in controlling vaccinia virus replication in C elegans.
URI: http://hdl.handle.net/11455/71171
ISSN: 0027-8424
文章連結: http://dx.doi.org/10.1073/pnas.0506442103
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