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Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
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Glucocorticosteroids increase cell entry by hepatitis C virus.

Sandra Ciesek1, Eike Steinmann, Markus Iken

  • 1Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany.

Gastroenterology
|February 16, 2010
PubMed
Summary
This summary is machine-generated.

Glucocorticosteroids enhance hepatitis C virus (HCV) entry into liver cells by increasing occludin and scavenger receptor expression. This suggests a mechanism for increased HCV dissemination in patients treated with these immunosuppressants.

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Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • Corticosteroids are vital immunosuppressants for autoimmune disorders and organ transplantation.
  • These drugs are known to exacerbate hepatitis C virus (HCV) recurrence post-liver transplant.
  • This suggests a direct role for corticosteroids in worsening HCV infection.

Purpose of the Study:

  • To investigate the impact of immunosuppressive drugs on HCV replication, assembly, and entry.
  • To elucidate the specific mechanisms by which corticosteroids affect HCV infection dynamics.

Main Methods:

  • HCV replication, assembly, and entry were assessed in cell culture models (Huh-7.5 cells) and primary human hepatocytes.
  • HCV RNA replication quantified using various assays (immunofluorescence, luciferase, qRT-PCR, ELISA).
  • Expression of host cell entry factors (occludin, SR-BI) analyzed via flow cytometry and immunoblotting.

Main Results:

  • Glucocorticosteroids marginally decreased HCV RNA replication but significantly increased HCV entry efficiency (up to 10-fold).
  • This effect was specific to HCV and not observed with other viruses.
  • Increased entry correlated with upregulated expression of occludin and scavenger receptor class B type I (SR-BI), key HCV entry factors.

Conclusions:

  • Glucocorticosteroids specifically enhance HCV entry by upregulating occludin and SR-BI.
  • These findings provide a mechanistic explanation for increased HCV dissemination in patients receiving high-dose glucocorticosteroids.