Key result
Activation of the interferon-inducible protein kinase PKR inhibits EMCV IRES-driven nonstructural protein synthesis from a subgenomic HCV clone through mechanisms independent of eIF-2 alpha phosphorylation.
Population
Human hepatoma Huh7 cells containing a subgenomic hepatitis C virus (HCV) replicon (pFKI389-NS3-3')
Comparison
Interferon-alpha treatment and transient… vs Untreated cells or absence of PKR overexpression
Design
Preclinical
Authors
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PKR modulation of HCV protein synthesis may warrant further mechanistic study; leaves open antiviral translation from animal data.
PKR assumes multiple roles in modulating HCV replication and protein synthesis, suggesting that tight control of PKR activity helps the virus evade the host's interferon system.
Rivas et al. (2002) studied Hepatitis C Virus (HCV) infection (in vitro model). PKR activation / IFN-alpha treatment vs. Untreated cells / PKR mutants was evaluated on Viral RNA replication and nonstructural (NS) protein expression. Activation of the interferon-inducible protein kinase PKR inhibits EMCV IRES-driven nonstructural protein synthesis from a subgenomic HCV clone through mechanisms independent of eIF-2 alpha phosphorylation.
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