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Atorvastatin Does Not Inhibit HCV Replication at Normal Doses

In July 2006, researchers reported data from a laboratory study showing that HMG-CoA reductase inhibitors -- better known as statins -- suppressed replication in an HCV "replicon" system. Statins are widely used to manage elevated blood cholesterol. According to a study published in the April 2007 issue of Hepatology, however, statins may not be active against HCV in patients at the doses typically used.

Researchers at Harvard Medical School and Massachusetts General Hospital in Boston designed a small prospective pilot clinical trial to evaluate the effect of one such agent -- atorvastatin (Lipitor) -- on HCV RNA levels. In this study, 10 HCV-infected patients who required treatment for high cholesterol received 20 mg atorvastatin daily.

The investigators reported that while total serum cholesterol and low-density lipoprotein (LDL or "bad" cholesterol) decreased significantly, as expected, there was "no statistically significant change" in HCV RNA levels at week 4 or week 12 compared with baseline levels.

In conclusion, the authors wrote, "atorvastatin, and likely all HMG-CoA reductase inhibitors, does not inhibit HCV RNA replication in vivo at conventional doses."
They added that, "It is unclear whether the addition of an HMG-CoA reductase inhibitor to interferon or a more potent inhibitor of cholesterol biosynthesis may be required to inhibit HCV RNA replication in vivo."

The earlier laboratory study used interferon plus statins to inhibit HCV replication. Atorvastatin was one of 2 statins that showed moderate anti-HCV inhibitory activity. Fluvastatin (Lescol) demonstrated the strongest inhibitory activity, while pravastatin (Pravachol) showed no anti-HCV activity.



JG O'Leary, JL Chan, CM McMahon, and others. Atorvastatin does not exhibit antiviral activity against HCV at conventional doses: A pilot clinical trial. Hepatology 45(4): 895-898. April 2007.