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Herpes simplex virus ICP0 mutants are hypersensitive to interferon.

K L Mossman1, H A Saffran, J R Smiley

  • 1Department of Medical Microbiology & Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.

Journal of Virology
|January 22, 2000
PubMed
Summary

Herpes simplex virus type 1 (HSV-1) requires the ICP0 protein to resist interferon (IFN) inhibition. Inactivating ICP0 makes HSV-1 highly sensitive to IFN, severely limiting viral replication and spread.

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Interferon (IFN) is a key immune molecule inducing antiviral states in cells.
  • Herpes simplex virus type 1 (HSV-1) replication is partially inhibited by IFN, likely via reduced viral transcription.

Purpose of the Study:

  • To investigate the role of HSV-1 immediate-early (IE) gene product ICP0 in IFN resistance.
  • To identify specific HSV-1 genes involved in overcoming IFN-mediated inhibition.

Main Methods:

  • Generating HSV-1 mutants with inactivated genes, including ICP0, VP16, vhs, ICP22, and UL13.
  • Assessing viral mRNA transcript and polypeptide levels in the presence of IFN.
  • Evaluating viral plaque formation ability in IFN-treated cells, including U2OS cells.

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Main Results:

  • Mutations inactivating ICP0 rendered HSV-1 exquisitely sensitive to IFN inhibition.
  • ICP0 inactivation led to decreased viral transcripts, polypeptides, and plaque formation.
  • Mutations in VP16, vhs, ICP22, and UL13 genes did not confer increased IFN sensitivity.
  • ICP0 mutants showed similar IFN sensitivity to wild-type virus in U2OS cells.

Conclusions:

  • Functional ICP0 is essential for HSV-1 to efficiently evade IFN-mediated antiviral effects in certain cell types.
  • ICP0 plays a critical role in overcoming IFN-induced cellular defenses for successful HSV-1 replication.