Hepatitis C virus NS5A protein inhibits interferon antiviral activity, but the effects do not correlate with clinical response

Gastroenterology. 1999 Nov;117(5):1187-97. doi: 10.1016/s0016-5085(99)70405-1.

Abstract

Background & aims: Patients with chronic hepatitis C virus infection are commonly treated with interferon alfa (IFN-alpha), but the long-term response rate is poor. A region of NS5A of hepatitis C virus genotype 1 (the ISDR) has been associated with treatment outcome in some patients. NS5A binds to and inhibits PKR in vitro and inhibits IFN-alpha in human cells. We examined the effects of the NS5A protein from patients who did or did not respond to IFN-alpha to determine whether NS5A from IFN-alpha nonresponders inhibited the effects of IFN-alpha in vitro.

Methods: We cloned NS5A from patients who had well-characterized responses to IFN-alpha and expressed them in a human fibroblast cell line under the control of an inducible promoter. The NS5A expression levels were controlled, and the effects of different proteins on the protective actions of IFN-alpha against encephalomyocarditis virus were investigated.

Results: NS5A expression blocked the antiviral effects of IFN-alpha in human cells. This inhibition was dependent on the level of NS5A expression. Although ISDR changes gave only small differences in IFN-alpha inhibition, clones derived from a patient who did not respond to IFN-alpha and one who did respond to treatment differed greatly: the clones from a patient with response to IFN-alpha were much more inhibitory than those derived from the patient with no response.

Conclusions: The inhibition of the antiviral effects of IFN-alpha by NS5A is not regulated exclusively by the ISDR, and the effects of NS5A in vitro do not correlate with treatment outcomes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / antagonists & inhibitors*
  • Antiviral Agents / pharmacology
  • Antiviral Agents / therapeutic use
  • Cell Line
  • Dose-Response Relationship, Drug
  • Drug Resistance
  • Encephalomyocarditis virus / drug effects
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Fibroblasts / virology
  • Hepatitis C, Chronic / blood
  • Humans
  • Interferon-alpha / antagonists & inhibitors*
  • Interferon-alpha / pharmacology
  • Interferon-alpha / therapeutic use
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • RNA, Messenger / metabolism
  • Transcription, Genetic / drug effects
  • Transfection
  • Viral Nonstructural Proteins / blood
  • Viral Nonstructural Proteins / chemistry
  • Viral Nonstructural Proteins / metabolism
  • Viral Nonstructural Proteins / pharmacology*

Substances

  • Antiviral Agents
  • Interferon-alpha
  • Peptide Fragments
  • RNA, Messenger
  • Viral Nonstructural Proteins
  • NS-5 protein, hepatitis C virus

Associated data

  • GENBANK/AJ133096
  • GENBANK/AJ133097
  • GENBANK/AJ133098
  • GENBANK/AJ133099