RGD Reference Report - Interferon-regulated pathways that control hepatitis B virus replication in transgenic mice. - Rat Genome Database

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Interferon-regulated pathways that control hepatitis B virus replication in transgenic mice.

Authors: Guidotti, Luca G  Morris, Amber  Mendez, Heike  Koch, Rick  Silverman, Robert H  Williams, Bryan R G  Chisari, Francis V 
Citation: Guidotti LG, etal., J Virol. 2002 Mar;76(6):2617-21. doi: 10.1128/jvi.76.6.2617-2621.2002.
RGD ID: 40902828
Pubmed: PMID:11861827   (View Abstract at PubMed)
PMCID: PMC135990   (View Article at PubMed Central)
DOI: DOI:10.1128/jvi.76.6.2617-2621.2002   (Journal Full-text)

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.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
EIF2AK2Humanhepatitis B disease_progressionIMP  RGD 
Eif2ak2Rathepatitis B disease_progressionISOEIF2AK2 (Homo sapiens) RGD 
Eif2ak2Mousehepatitis B disease_progressionISOEIF2AK2 (Homo sapiens) RGD 
IRF1Humanhepatitis B disease_progressionISOIrf1 (Mus musculus) RGD 
Irf1Rathepatitis B disease_progressionISOIrf1 (Mus musculus) RGD 
Irf1Mousehepatitis B disease_progressionIMP  RGD 
RNASELHumanhepatitis B  ISORnasel (Mus musculus) RGD 
RnaselRathepatitis B  ISORnasel (Mus musculus) RGD 
RnaselMousehepatitis B  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Eif2ak2  (eukaryotic translation initiation factor 2-alpha kinase 2)
Irf1  (interferon regulatory factor 1)
Rnasel  (ribonuclease L)

Genes (Mus musculus)
Eif2ak2  (eukaryotic translation initiation factor 2-alpha kinase 2)
Irf1  (interferon regulatory factor 1)
Rnasel  (ribonuclease L (2', 5'-oligoisoadenylate synthetase-dependent))

Genes (Homo sapiens)
EIF2AK2  (eukaryotic translation initiation factor 2 alpha kinase 2)
IRF1  (interferon regulatory factor 1)
RNASEL  (ribonuclease L)


Additional Information