AI Article Synopsis

  • Statins are primarily used to lower cholesterol but also show potential antiviral activity against hepatitis C virus (HCV).
  • Their antiviral mechanism may involve inhibiting the geranylgeranylation of cellular proteins rather than simply reducing cholesterol levels.
  • While statins alone are not enough to treat chronic HCV, combining them with standard therapies improves treatment success rates without causing extra side effects.

Article Abstract

Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors that are widely used for the treatment of hypercholesterolemia. Besides their cholesterol-lowering effect, statins have been reported to have antiviral activity against a variety of viruses, including hepatitis C virus (HCV). Several statins inhibit the in vitro replication of subgenomic HCV replicons and also suppress in vitro RNA replication of infectious HCV. The precise mechanism of the anti-HCV activity of statins has not yet been defined. Recent studies suggest that the antiviral effect may result from the inhibition of geranylgeranylation of cellular proteins, rather than the inhibition of cholesterol synthesis. Despite the antiviral effect observed in vitro, statin monotherapy seems to be insufficient for the treatment of chronic HCV infection. However, several prospective and retrospective studies have demonstrated that the addition of statins to IFN-α and ribavirin therapy increases SVR, RVR, and EVR rates without the occurrence of additional adverse events. These clinical data, together with the excellent safety profile and low cost, suggest that statins may play a role in HCV therapy until more potent and safe direct-acting antivirals become available. This article forms part of a symposium in Antiviral Research on "Hepatitis C: next steps toward global eradication."

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Source
http://dx.doi.org/10.1016/j.antiviral.2014.02.020DOI Listing

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