Restriction of vaccinia virus replication by a ced-3 and ced-4-dependent pathway in Caenorhabditis elegans
Journal
Proceedings of the National Academy of Sciences of the United States of America
Journal Volume
103
Journal Issue
11
Pages
4174 - 4179
Date Issued
2006
Author(s)
Abstract
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, ced-9(gf), and egl-1(If) mutants, demonstrating that the core programmed cell death (PCD) genes ced-3, ced-4, ced-3, 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. ? 2006 by The National Academy of Sciences of the USA.
Subjects
Programmed cell death; Virus-host interaction
SDGs
Other Subjects
allele; apoptosis; article; Caenorhabditis elegans; ced 3 gene; ced 4 gene; ced 9 gene; cell division; cell killing; controlled study; cul 1 gene; egl 1 gene; gene; gene function; gene mutation; gene overexpression; genetic manipulation; host pathogen interaction; icd 1 gene; lin 23 gene; nonhuman; priority journal; Vaccinia virus; virus cell interaction; virus replication; Animals; Apoptosis; Apoptosis Regulatory Proteins; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Calcium-Binding Proteins; Caspases; Genes, Helminth; Mutation; Proto-Oncogene Proteins; Repressor Proteins; Vaccinia virus; Virus Replication; Bacteria (microorganisms); Caenorhabditis elegans; Nematoda; Vaccinia virus
Type
journal article