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- W2083626719 abstract "ABSTRACT The VP35 protein of Zaire Ebola virus is an essential component of the viral RNA polymerase complex and also functions to antagonize the cellular type I interferon (IFN) response by blocking activation of the transcription factor IRF-3. We previously mapped the IRF-3 inhibitory domain within the C terminus of VP35. In the present study, we show that mutations that disrupt the IRF-3 inhibitory function of VP35 do not disrupt viral transcription/replication, suggesting that the two functions of VP35 are separable. Second, using reverse genetics, we successfully recovered recombinant Ebola viruses containing mutations within the IRF-3 inhibitory domain. Importantly, we show that the recombinant viruses were attenuated for growth in cell culture and that they activated IRF-3 and IRF-3-inducible gene expression at levels higher than that for Ebola virus containing wild-type VP35. In the context of Ebola virus pathogenesis, VP35 may function to limit early IFN-β production and other antiviral signals generated from cells at the primary site of infection, thereby slowing down the host's ability to curb virus replication and induce adaptive immunity." @default.
- W2083626719 created "2016-06-24" @default.
- W2083626719 creator A5014946505 @default.
- W2083626719 creator A5061775143 @default.
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- W2083626719 date "2006-07-01" @default.
- W2083626719 modified "2023-10-17" @default.
- W2083626719 title "Reverse Genetic Generation of Recombinant Zaire Ebola Viruses Containing Disrupted IRF-3 Inhibitory Domains Results in Attenuated Virus Growth In Vitro and Higher Levels of IRF-3 Activation without Inhibiting Viral Transcription or Replication" @default.
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- W2083626719 doi "https://doi.org/10.1128/jvi.00044-06" @default.
- W2083626719 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1488969" @default.
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