pubmed-article:11861827 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C0019169 | lld:lifeskim |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C0042774 | lld:lifeskim |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:11861827 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:11861827 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:11861827 | pubmed:dateCreated | 2002-2-25 | lld:pubmed |
pubmed-article:11861827 | pubmed:abstractText | We previously showed that the intrahepatic induction of cytokines such as alpha/beta interferon (IFN-alpha/beta) and gamma interferon (IFN-gamma) inhibits hepatitis B virus (HBV) replication noncytopathically in the livers of transgenic mice. The intracellular pathway(s) responsible for this effect is still poorly understood. To identify interferon (IFN)-inducible intracellular genes that could play a role in our system, we crossed HBV transgenic mice with mice deficient in IFN regulatory factor 1 (IRF-1), the double-stranded RNA-activated protein kinase (PKR), or RNase L (RNase L) (IRF-1(-/-), PKR(-/-), or RNase L(-/-) mice, respectively), three well-characterized IFN-inducible genes that mediate antiviral activity. We showed that unmanipulated IRF-1(-/-) or PKR(-/-) transgenic mice replicate HBV in the liver at slightly higher levels than the respective controls, suggesting that both IRF-1 and PKR individually appear to mediate signals that modulate HBV replication under basal conditions. These same animals were responsive to the antiviral effects of the IFN-alpha/beta inducer poly(I-C) or recombinant murine IFN-gamma, suggesting that under these conditions, either the IRF-1 or the PKR genes can mediate the antiviral activity of the IFNs or other IFN-inducible genes mediate the antiviral effects. Finally, RNase L(-/-) transgenic mice were undistinguishable from controls under basal conditions and after poly(I-C) or IFN-gamma administration, suggesting that RNase L does not modulate HBV replication in this model. | lld:pubmed |
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pubmed-article:11861827 | pubmed:language | eng | lld:pubmed |
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pubmed-article:11861827 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11861827 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11861827 | pubmed:month | Mar | lld:pubmed |
pubmed-article:11861827 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:WilliamsBryan... | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:SilvermanRobe... | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:ChisariFranci... | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:GuidottiLuca... | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:MorrisAmberA | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:MendezHeikeH | lld:pubmed |
pubmed-article:11861827 | pubmed:author | pubmed-author:KochRickR | lld:pubmed |
pubmed-article:11861827 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11861827 | pubmed:volume | 76 | lld:pubmed |
pubmed-article:11861827 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11861827 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11861827 | pubmed:pagination | 2617-21 | lld:pubmed |
pubmed-article:11861827 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:11861827 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11861827 | pubmed:articleTitle | Interferon-regulated pathways that control hepatitis B virus replication in transgenic mice. | lld:pubmed |
pubmed-article:11861827 | pubmed:affiliation | Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. guidotti@scripps.edu | lld:pubmed |
pubmed-article:11861827 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11861827 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11861827 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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