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Inhibition of viral assembly in murine cells by HIV-1 matrix

Wolfgang Hübner1, Benjamin K Chen

  • 1Department of Pharmacology and Biological Chemistry, Center for Immunobiology, Mount Sinai School of Medicine, One Gustave Levy Place Box 1215, New York, NY 10029, USA.

Virology
|June 6, 2006
PubMed

Insights

Murine leukemia virus (MLV) matrix (MA) enhances human immunodeficiency virus type 1 (HIV-1) Gag membrane binding in murine cells. However, efficient HIV-1 assembly requires removing HIV-1 MA and involves host factors interacting with MA's globular head.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • The N-terminal matrix (MA) domain of human immunodeficiency virus type 1 (HIV-1) Gag is crucial for targeting viral assembly to specific cellular membrane compartments.
  • HIV-1 Gag assembly and membrane targeting are inefficient in murine fibroblasts compared to human cells.
  • Chimeric proviruses with murine leukemia virus (MLV) MA can rescue these deficiencies.

Purpose of the Study:

  • To investigate the role of MLV MA in enhancing HIV-1 Gag membrane binding and assembly in murine cells.
  • To determine the specific domains of MA involved in cell-type-specific assembly phenotypes.
  • To elucidate the interaction between MA and host factors in regulating viral assembly.

Main Methods:

  • Construction and analysis of chimeric HIV-1 proviruses containing tandem MLV and HIV-1 MA domains.
  • Assessment of Gag membrane binding efficiency in murine cells.
  • Evaluation of Gag processing and virus production in murine cells.
  • Site-directed mutagenesis to delete the globular head of MA.

Main Results:

  • Addition of MLV MA to HIV-1 Gag enhanced membrane binding in murine cells but did not fully restore virus production.
  • Removal of HIV-1 MA was necessary for efficient Gag processing and increased virus production in murine cells.
  • Deletion of the MA globular head partially restored membrane binding and Gag processing but did not enhance virus production.

Conclusions:

  • MA-dependent, cell-type-specific phenotypes indicate a complex regulation of HIV-1 assembly.
  • Host factors likely interact with the globular head of MA to regulate membrane binding.
  • Additional membrane-independent steps are critical for efficient viral assembly, influenced by MA-host factor interactions.

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