Impact of Vesicular Stomatitis Virus M Proteins on Different Cellular Functions

Natalia Redondo1, Vanesa Madan2, Enrique Alvarez1

  • 1Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Nicolás Cabrera 1, Campus de Cantoblanco, Madrid, Spain.

Plos One
|June 20, 2015
PubMed

Insights

Vesicular stomatitis virus (VSV) matrix proteins M1, M2, and M3 disrupt host cell functions. These viral proteins inhibit cellular protein synthesis and mRNA transport, impacting cell viability and viral replication.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Vesicular stomatitis virus (VSV) possesses three distinct matrix (M) proteins: M1, M2, and M3.
  • The functions and cellular impacts of these VSV M proteins are not fully elucidated.

Purpose of the Study:

  • To investigate the individual and shared cellular effects of VSV M1, M2, and M3 proteins.
  • To understand the mechanisms by which these viral proteins interfere with host cell processes.

Main Methods:

  • Expression of individual VSV M proteins (M1, M2, M3) in host cells.
  • Analysis of cytopathic effects, including cell morphology and protein synthesis.
  • Assessment of viral particle budding and plasma membrane permeability.
  • Investigation of mRNA transport and splicing factor redistribution.

Main Results:

  • Individual expression of M1, M2, and M3 induced cytopathic effects like cell rounding and detachment.
  • VSV M proteins partially inhibited cellular protein synthesis via an indirect mechanism.
  • M1 promoted virus particle budding without increasing membrane permeability.
  • M2 and M3 did not interact with the cellular membrane or induce vesicle budding.
  • All three M proteins interfered with nuclear mRNA export and modulated splicing factor localization.

Conclusions:

  • VSV M1, M2, and M3 proteins exhibit distinct and shared activities that disrupt host cell functions.
  • These viral proteins significantly impact host cell machinery, including protein synthesis and mRNA transport.
  • Understanding these interactions is crucial for comprehending VSV pathogenesis and developing antiviral strategies.

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