Journal
JOURNAL OF VIROLOGY
Volume 76, Issue 6, Pages 2617-2621Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.76.6.2617-2621.2002
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Funding
- NATIONAL CANCER INSTITUTE [R01CA044059, R37CA040489, R01CA040489] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI040696, R01AI034039, R21AI034039] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA040489, R01 CA044059, R37 CA040489, CA40489, CA44059] Funding Source: Medline
- NIAID NIH HHS [R01 AI040696, R01 AI034039, AI40696, AI34039] Funding Source: Medline
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We previously showed that the intrahepatic induction of cytokines such as alpha/beta interferon (IFN-alpha/beta) and gamma interferon (ITN-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.
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