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Cell-specific inhibition of paramyxovirus maturation by proteasome inhibitors

Hitoshi Watanabe1, Yoshikazu Tanaka, Yukie Shimazu

  • 1Department of Virology, Graduate School of Biomedical Sciences, Hiroshima University 1-2-3 Kasumi, Minami-ku, Hiroshima, Japan.

Microbiology and Immunology
|September 21, 2005
PubMed

Insights

Proteasome inhibitors significantly impede Sendai virus (SeV) replication and maturation by disrupting early assembly steps. This antiviral effect is highly cell-specific and virus-specific, impacting paramyxoviruses more than orthomyxoviruses or rhabdoviruses.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Proteasomes play crucial roles in cellular protein degradation.
  • The impact of proteasome inhibitors on paramyxovirus replication is not fully understood.
  • Investigating drug effects on viral replication aids in developing antiviral strategies.

Purpose of the Study:

  • To investigate the effects of proteasome inhibitors on Sendai virus (SeV) replication.
  • To compare these effects with those on orthomyxovirus and rhabdovirus replication.
  • To elucidate the specific stages of viral replication affected by proteasome inhibition.

Main Methods:

  • LLC-MK2 cells infected with Sendai virus (SeV) were treated with MG132, Lactacystin, and zLL.
  • Viral protein levels and infectivity were measured.
  • An SeV-like particle formation system was used to assess virus maturation.
  • Cell-specific effects were evaluated using CV1 and A549 cells.
  • Comparative studies included vesicular stomatitis virus and influenza virus A/WSN/33.

Main Results:

  • MG132 significantly reduced SeV growth in a dose-dependent manner, decreasing viral protein release and infectivity.
  • Proteasome inhibition disturbed early SeV assembly, affecting M protein and glycoprotein localization.
  • Virus maturation was impaired, as confirmed by the SeV-like particle system.
  • The susceptibility to MG132 varied significantly across different cell types (LLC-MK2, CV1, A549) and viruses (SeV, vesicular stomatitis virus, influenza virus).

Conclusions:

  • Proteasome inhibitors disrupt early Sendai virus assembly and maturation.
  • The antiviral efficacy of proteasome inhibitors is both cell-specific and virus-specific.
  • These findings highlight the potential of targeting proteasomes for antiviral therapy, with careful consideration of host cell and viral factors.

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