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The herpes simplex virus regulatory protein ICP27 contributes to the decrease in cellular mRNA levels during

M A Hardwicke1, R M Sandri-Goldin

  • 1Department of Microbiology and Molecular Genetics, College of Medicine, University of California, Irvine 92717-4025.

Journal of Virology
|August 1, 1994
PubMed
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Herpes simplex virus protein ICP27 impairs host cell splicing, reducing cellular mRNA levels during infection. ICP27 is essential for this effect, impacting viral replication and host gene expression.

Area of Science:

  • Virology
  • Molecular Biology
  • Gene Expression

Background:

  • Herpes simplex virus (HSV) immediate-early protein ICP27 is known to regulate gene expression posttranscriptionally.
  • Previous studies indicated ICP27 affects mRNA processing, decreasing spliced target mRNAs in transfection assays.
  • ICP27 is also implicated in the "host shutoff" phenomenon observed during HSV infection.

Purpose of the Study:

  • To investigate the role of ICP27 in modulating the accumulation of spliced cellular mRNAs during herpes simplex virus type 1 (HSV-1) infection.
  • To determine if ICP27 contributes to the reduction of cellular mRNA levels by affecting host cell splicing.
  • To elucidate the mechanism by which ICP27 influences host mRNA processing during viral infection.

Main Methods:

  • Utilized HSV-1 viral mutants defective in ICP27 expression.

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  • Performed infections with wild-type HSV-1 and ICP27 mutant viruses.
  • Conducted nuclear runoff transcription assays to differentiate transcriptional and posttranscriptional effects.
  • Analyzed the accumulation levels of spliced host mRNAs and precursor mRNAs.

    • Main Results:

    • Infections with ICP27-defective viral mutants showed higher accumulated levels of spliced host mRNAs compared to wild-type HSV-1 infections.
    • Nuclear runoff assays confirmed that the observed differences in mRNA levels occurred posttranscriptionally.
    • The stability of spliced mRNA products was similar between wild-type and ICP27 mutant infections.
    • Unspliced precursor mRNA for a viral gene was detected during wild-type HSV-1 infection but not when ICP27 was absent.

    Conclusions:

    • ICP27 plays a critical role in reducing cellular mRNA levels during HSV-1 infection.
    • The reduction in cellular mRNA and accumulation of pre-mRNA are linked and likely caused by ICP27-mediated impairment of host cell splicing.
    • ICP27 is required for the observed effects on host cell mRNA processing and accumulation.