Abstract
Wolbachia blocks dengue virus replication in Drosophila melanogaster as well as in Aedes aegypti. Using the Drosophila model and mutations in the Toll and Imd pathways, we showed that neither pathway is required for expression of the dengue virus-blocking phenotype in the Drosophila host. This provides additional evidence that the mechanistic basis of Wolbachia-mediated dengue virus blocking in insects is more complex than simple priming of the host insect innate immune system.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Dengue Virus / growth & development*
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Drosophila Proteins / genetics
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Drosophila Proteins / immunology*
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Drosophila melanogaster / immunology
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Drosophila melanogaster / microbiology*
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Drosophila melanogaster / virology*
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Female
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Immunity, Innate
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Microbial Interactions*
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Mutation
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Signal Transduction
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Toll-Like Receptors / genetics
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Toll-Like Receptors / immunology*
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Wolbachia / growth & development*
Substances
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Drosophila Proteins
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Tl protein, Drosophila
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Toll-Like Receptors
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imd protein, Drosophila