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The herpes simplex virus virion host shutoff function.

A D Kwong1, N Frenkel

  • 1Department of Molecular Genetics and Cell Biology, University of Chicago, Illinois 60637.

Journal of Virology
|November 1, 1989
PubMed
Summary
This summary is machine-generated.

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Herpes simplex virus (HSV) virion host shutoff (vhs) protein degrades cellular mRNA. A vhs-1 mutant protein can block this shutoff, suggesting a stoichiometric interaction with a cellular factor affecting mRNA stability.

Area of Science:

  • Virology
  • Molecular Biology
  • Gene Expression

Background:

  • Herpes simplex virus (HSV) employs a virion host shutoff (vhs) function to suppress host gene expression by mRNA destabilization.
  • Mutations in vhs can impair its mRNA degradation activity, leading to longer mRNA half-lives.
  • The vhs-1 mutation is located within the UL41 open reading frame.

Purpose of the Study:

  • To investigate the mechanism of HSV-1 virion host shutoff (vhs) function.
  • To analyze the interaction between wild-type (wt) HSV-1 and vhs-1 mutant viruses in host protein synthesis shutoff.
  • To elucidate the role of the vhs protein in regulating mRNA stability.

Main Methods:

  • Infection of cells with a mixture of wt HSV-1 (KOS) and the vhs-1 mutant virus.

Related Experiment Videos

  • Analysis of host protein synthesis shutoff.
  • Assessment of mRNA half-life in infected cells.

    • Main Results:

    • Wild-type HSV-1 shutoff activity requires a minimum number of input virions per cell.
    • The mutant vhs-1 protein can irreversibly inhibit the shutoff activity of the wt virus.
    • These findings support a stoichiometric model of vhs function.

    Conclusions:

    • The wt vhs protein interacts with a cellular factor to destabilize host and viral mRNAs.
    • The mutant vhs-1 protein irreversibly binds this cellular factor, stabilizing mRNAs.
    • This interaction mechanism regulates mRNA half-life during HSV infection.