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Atorvastatin does not exhibit antiviral activity against HCV at conventional doses: A pilot clinical trial
Author(s) -
O'Leary Jacqueline G.,
Chan Jessica L.,
McMahon Cory M.,
Chung Raymond T.
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.21554
Subject(s) - atorvastatin , in vivo , rna , reductase , hmg coa reductase , cholesterol , in vitro , pharmacology , medicine , viral replication , hydroxymethylglutaryl coa reductase , virology , biology , enzyme , biochemistry , virus , gene , microbiology and biotechnology
Abstract Cholesterol biosynthesis is an integral part of HCV RNA replication. Not only does HCV RNA replicate on lipid rafts, but it also requires cholesterol intermediates to replicate. In addition, it has been shown in vitro that several HMG‐CoA reductase inhibitors can decrease HCV RNA replication by ≥ 1 log. Therefore, we designed a clinical trial to evaluate the effect of atorvastatin on HCV RNA levels. In this prospective clinical trial, where patients served as their own control, 10 HCV‐infected patients who required treatment for high cholesterol were given 20 mg atorvastatin per day. Although serum cholesterol and LDL predictably decreased significantly, there was no statistically significant change in week 4 and week 12 HCV RNA levels compared to pretreatment HCV RNA levels by the paired Student t test. 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 . In conclusion, atorvastatin, and likely all HMG‐CoA reductase inhibitors, does not inhibit HCV RNA replication in vivo at conventional doses. (H EPATOLOGY 2007;45:895–898.)