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Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function

Sarah A Kopecky-Bromberg1, Luis Martínez-Sobrido, Matthew Frieman

  • 1Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.

Journal of Virology
|November 17, 2006
PubMed

Insights

Severe acute respiratory syndrome coronavirus (SARS-CoV) proteins ORF 3b, ORF 6, and N antagonize the host's interferon response. These viral proteins inhibit interferon synthesis and signaling through distinct mechanisms, aiding SARS-CoV pathogenicity.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic human virus.
  • Understanding viral mechanisms to overcome host innate immunity is crucial.

Purpose of the Study:

  • To investigate how SARS-CoV proteins antagonize the interferon response.
  • To elucidate the specific roles of SARS-CoV ORF 3b, ORF 6, and N proteins in immune evasion.

Main Methods:

  • Assessing the impact of SARS-CoV ORF 3b, ORF 6, and N proteins on interferon-beta (IFN-beta) expression.
  • Analyzing the inhibition of IRF-3, a key protein for IFN-beta expression.
  • Evaluating promoter activity using NF-kappaB and interferon-stimulated response element (ISRE) reporters.
  • Investigating STAT1 phosphorylation and nuclear translocation.

Main Results:

  • SARS-CoV ORF 3b, ORF 6, and N proteins inhibit IFN-beta expression by targeting IRF-3.
  • N protein inhibits expression from an NF-kappaB-responsive promoter.
  • All three proteins inhibit ISRE promoter activity after viral infection; ORF 3b and ORF 6 also inhibit it after interferon treatment.
  • ORF 3b and ORF 6 inhibit both interferon synthesis and signaling, while N protein primarily inhibits synthesis.
  • ORF 6 inhibits STAT1 nuclear translocation but not phosphorylation.

Conclusions:

  • SARS-CoV utilizes ORF 3b, ORF 6, and N proteins as distinct interferon antagonists.
  • These proteins employ different strategies to disrupt the host interferon response, contributing to viral pathogenicity.

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