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Genetic inactivation of COPI coatomer separately inhibits vesicular stomatitis virus entry and gene expression

David K Cureton1, Rebeca Burdeinick-Kerr, Sean P J Whelan

  • 1Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA. cureton@idi.harvard.edu

Journal of Virology
|November 11, 2011
PubMed

Insights

Disrupting the COPI coatomer complex, essential for membrane transport, blocks vesicular stomatitis virus (VSV) entry and replication. Prolonged COPI inactivation impairs viral gene expression and cell invasion.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Viruses utilize host cell membrane transport for invasion, replication, and release.
  • Genome-wide screens indicate diverse viruses depend on COPI coatomer complex for replication.

Purpose of the Study:

  • To investigate the role of COPI coatomer complex in vesicular stomatitis virus (VSV) replication.
  • To determine specific replication stages affected by COPI inactivation.

Main Methods:

  • Utilized RNA interference (RNAi) to deplete the ε-COP subunit of the COPI complex.
  • Employed visual and biochemical assays to measure viral entry and gene expression.
  • Applied brefeldin A (BFA) to inhibit COPI function and assess its impact on VSV.

Main Results:

  • ε-COP depletion for 12 hours primarily blocked VSV internalization and secondarily impaired gene expression.
  • Short-term BFA treatment inhibited VSV gene expression, while long-term treatment blocked viral entry.
  • Prolonged COPI inactivation was shown to indirectly impair VSV entry by perturbing endocytic transport.

Conclusions:

  • COPI coatomer complex is crucial for VSV entry, with prolonged inactivation affecting endocytic transport.
  • The findings explain COPI's frequent identification in screens for cellular factors supporting pathogen invasion.

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