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Matrix fibronectin binds gammaretrovirus and assists in entry: new light on viral infections

Christiane Beer1, Lene Pedersen

  • 1Department of Molecular Biology, Aarhus University, C. F. Møllers Allé, Building 130, DK-8000 Aarhus C, Denmark.

Journal of Virology
|May 25, 2007
PubMed

Insights

Amphotropic murine leukemia virus (A-MLV) uses the fibronectin matrix to enter cells via caveola-dependent endocytosis. Inhibiting this viral binding significantly reduced infection, highlighting fibronectin's active role.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Amphotropic murine leukemia virus (A-MLV) enters NIH 3T3 fibroblasts through caveola-dependent endocytosis.
  • Few viral particles are typically observed intracellularly during infection.
  • The role of the extracellular matrix in viral entry remains incompletely understood.

Purpose of the Study:

  • To investigate the dynamics of A-MLV infection and the role of the fibronectin matrix.
  • To elucidate the cellular uptake pathway of A-MLV in relation to fibronectin.

Main Methods:

  • Total internal reflection fluorescence microscopy to analyze viral dynamics.
  • Confocal microscopy to track nanoparticle and viral colocalization.
  • Inhibition of viral binding to fibronectin to assess infection rates.

Main Results:

  • The majority of A-MLV particles were found extracellularly, bound to the fibronectin matrix.
  • A correlation was observed between bound virus amounts and fibronectin levels.
  • Fibronectin-targeted nanoparticles were internalized by NIH 3T3 cells, colocalizing with A-MLV.
  • Inhibiting viral binding to fibronectin significantly reduced A-MLV infection.

Conclusions:

  • Fibronectin matrix binding is a crucial mechanism for A-MLV cell entry.
  • A-MLV utilizes caveola-dependent endocytosis, engaging with the fibronectin matrix.
  • This interaction plays an active and significant role in the viral infection process.

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