Role of matrix protein in cytopathogenesis of vesicular stomatitis virus

D Blondel1, G G Harmison, M Schubert

  • 1Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892.

Journal of Virology
|April 1, 1990
PubMed

Insights

The matrix (M) protein of vesicular stomatitis virus (VSV) causes visible cell damage (cytopathic effects, CPE) by disrupting the cytoskeleton. This CPE is reversible and directly linked to M protein function.

Area of Science:

  • Virology
  • Cell Biology

Background:

  • The matrix (M) protein of vesicular stomatitis virus (VSV) is crucial for viral assembly and transcription.
  • VSV infection typically induces cytopathic effects (CPE), including cell rounding.

Purpose of the Study:

  • To investigate the role of the VSV M protein in causing CPE.
  • To determine if M protein alone can induce cellular morphological changes.

Main Methods:

  • Analysis of a temperature-sensitive VSV M protein mutant (tsG33).
  • Microinjection of antisense oligonucleotides targeting M protein.
  • Transfection of cells with cDNA encoding the tsG33 M protein.

Main Results:

  • The tsG33 mutant M protein failed to induce CPE at the nonpermissive temperature but did so upon shifting to the permissive temperature.
  • Antisense inhibition of M protein translation prevented CPE.
  • Transfected cells expressing tsG33 M protein showed temperature-dependent CPE, including cell rounding and detachment.
  • Absence of CPE at nonpermissive temperature correlated with abnormal M protein localization, suggesting self-aggregation or membrane association.

Conclusions:

  • VSV M protein, independently of other viral proteins, induces cell rounding and detachment, likely via cytoskeletal disorganization.
  • The temperature-sensitive defect in M protein assembly and CPE is reversible.
  • Mutant M protein's altered localization at nonpermissive temperatures may explain its inability to induce CPE.

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