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Budding of PPxY-containing rhabdoviruses is not dependent on host proteins TGS101 and VPS4A

Takashi Irie1, Jillian M Licata, James P McGettigan

  • 1Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

Journal of Virology
|March 3, 2004
PubMed

Insights

Viral matrix proteins use late budding (L-domains) for virus assembly. This study found differences in budding efficiency between Ebola virus and vesicular stomatitis virus (VSV) L-domains, highlighting distinct host factor dependencies for virus budding.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Enveloped RNA viruses utilize matrix proteins for assembly and budding.
  • Late budding (L-domains) motifs (PT/SAP, PPxY, YxxL) mediate budding by interacting with cellular proteins.
  • These interactions suggest a role for vacuolar sorting and endocytic pathways in viral budding.

Purpose of the Study:

  • To compare the L-domain functions between Ebola virus VP40 and vesicular stomatitis virus (VSV) M protein.
  • To investigate the role of the PSAP motif in VSV M protein budding.
  • To elucidate the differential dependence on host factors for budding between PTAP and PPxY motif-containing viruses.

Main Methods:

  • Construction of a chimeric M protein (M40) replacing VSV M's PPPY motif with Ebola virus VP40 L-domains.
  • Assessing the budding efficiency of wild-type (wt) M protein and M40-containing virus-like particles (VLPs).
  • Evaluating the impact of VPS4A and TSG101 manipulation on VLP budding.

Main Results:

  • The chimeric M40 protein exhibited a 10-fold higher budding efficiency than wt M protein.
  • Overexpression of dominant-negative VPS4A or TSG101 depletion specifically inhibited M40 VLP budding.
  • Wt M VLPs and live VSV budding were unaffected by VPS4A or TSG101 manipulation.

Conclusions:

  • The PSAP motif in VSV M protein is not essential for viral budding.
  • Significant differences exist in host factor requirements for budding between PTAP-containing viruses (e.g., Ebola virus) and PPxY-containing viruses (e.g., VSV).
  • Viral budding mechanisms show distinct dependencies on cellular pathways like vacuolar sorting and endocytosis.

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