Statins can exert dual, concentration dependent effects on HCV entry in vitro

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Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

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Matthieu Blanchet1, Quoc-Tuan Le1, Nabil G Seidah2

  • 1INRS-Institut Armand-Frappier, Institut National de la Recherche Scientifique, Laval, Canada.

Antiviral Research
|February 13, 2016
PubMed

Insights

Statins may worsen Hepatitis C Virus (HCV) entry by increasing LDLR, but some statins also inhibit entry by downregulating CLDN-1 at higher doses. Pravastatin shows a purely proviral effect on HCV entry.

Area of Science:

  • Virology
  • Pharmacology
  • Biochemistry

Background:

  • Statins, primarily 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoAR) inhibitors, are widely used for hypercholesterolemia.
  • In vivo studies suggest statins may enhance sustained viral response (SVR) in Hepatitis C Virus (HCV) patients treated with PEG-IFN and ribavirin.

Purpose of the Study:

  • To investigate the in vitro effects of various statins on HCV entry.
  • To examine the impact of statins on key HCV entry factors, specifically LDLR and CLDN-1.

Main Methods:

  • In vitro assessment of statin effects on HCV entry.
  • Analysis of statin-induced changes in the expression of LDLR and CLDN-1.

Main Results:

  • All tested statins upregulated LDLR, suggesting a proviral effect on HCV entry.
  • At higher concentrations, statins (excluding pravastatin) downregulated CLDN-1, indicating a competing antiviral effect.
  • Pravastatin demonstrated a consistent proviral effect on HCV entry in vitro.

Conclusions:

  • Statins exhibit a dual effect on HCV entry in vitro: a proviral effect via LDLR upregulation and a potential antiviral effect via CLDN-1 downregulation (except for pravastatin).
  • Pravastatin's effect on HCV entry is predominantly proviral in vitro.

Keywords:
CD81CLDN-1CholesterolHCVLDLRLipidsNPC1L1PCSK9Statins

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