Potent inhibition of SARS-associated coronavirus (SCOV) infection and replication by type I interferons (IFN-alpha/beta) but not by type II interferon (IFN-gamma)

J Interferon Cytokine Res. 2004 Jul;24(7):388-90. doi: 10.1089/1079990041535610.

Abstract

We sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (alpha and beta) and type II (gamma) interferons (IFN) in vitro. Type I IFNs protected cells from cytopathic effects (CPE) induced by SCoV, and inhibited viral genomic RNA replication in FRhk-4 cells (measured by quantitative RT-PCR) in a dose-dependent manner. Intracellular viral RNA copies were reduced 50% by IFN-alpha at a concentration of 25 U/ml and by IFN-beta at a concentration of 14 U/ml. IFN-gamma had fewer effects on inhibition of viral infection and replication. The type I IFN receptor signaling pathway in host cells is mainly involved in the inhibition of SCoV infection and replication. Type I IFNs could be used as potential agents for anti-SARS treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology*
  • Cell Line
  • Cytopathogenic Effect, Viral / drug effects
  • Dose-Response Relationship, Drug
  • Humans
  • Interferon Type I / pharmacology*
  • Interferon-gamma / pharmacology*
  • RNA, Viral / biosynthesis*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Severe acute respiratory syndrome-related coronavirus* / metabolism
  • Severe acute respiratory syndrome-related coronavirus* / pathogenicity
  • Signal Transduction / drug effects
  • Virus Replication / drug effects*

Substances

  • Antiviral Agents
  • Interferon Type I
  • RNA, Viral
  • Interferon-gamma