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Murine leukemia virus glycosylated Gag (gPr80gag) facilitates interferon-sensitive virus release through lipid rafts

Takayuki Nitta1, Yurii Kuznetsov, Alexander McPherson

  • 1Department of Molecular Biology and Biochemistry, and Cancer Research Institute, University of California, Irvine, CA 92697-3905, USA.

Proceedings of the National Academy of Sciences of the United States of America
|January 19, 2010
PubMed

Insights

Murine leukemia viruses

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Murine leukemia viruses possess a unique glyco-gag protein (gPr80gag).
  • The precise function of gPr80gag in viral production has remained largely unknown.
  • gPr80gag is conserved across gammaretroviruses and implicated in late viral assembly or release steps.

Purpose of the Study:

  • To elucidate the mechanism by which gPr80gag facilitates murine leukemia virus release.
  • To investigate the role of lipid rafts in gPr80gag-mediated viral release.
  • To determine if gPr80gag can enhance the release of heterologous viral vectors.

Main Methods:

  • Analysis of Moloney murine leukemia virus (M-MuLV) release in gPr80gag-expressing and deficient cells.
  • Assessment of viral particle cholesterol content and sensitivity to MbetaCD.
  • Quantification of Pr65gag association with detergent-resistant membranes.
  • Evaluation of HIV-1-based vector release from 293T cells.

Main Results:

  • gPr80gag significantly facilitates M-MuLV release via an interferon-sensitive pathway.
  • gPr80gag-dependent release involves lipid rafts, evidenced by altered cholesterol content and MbetaCD sensitivity.
  • Absence of gPr80gag reduces Pr65gag association with detergent-resistant membranes.
  • gPr80gag enhances the release of HIV-1-based vector particles.

Conclusions:

  • gPr80gag plays a critical role in the efficient release of murine leukemia viruses.
  • Lipid raft-mediated mechanisms are essential for gPr80gag-facilitated viral release.
  • gPr80gag has potential applications in enhancing the production of lentiviral vectors.

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