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ESCRT requirements for EIAV budding.

Virginie Sandrin1, Wesley I Sundquist

  • 1Department of Biochemistry, University of Utah School of Medicine, Salt Lake City 84112-5650, Utah, USA. wes@biochem.utah.edu.

Retrovirology
|October 11, 2013
PubMed
Summary
This summary is machine-generated.

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Equine Infectious Anemia Virus (EIAV) budding requires a specific ESCRT protein network, including ALIX, CHMP4B, CHMP2A, and VPS4. CHMP4B controls virion assembly and membrane fission during budding.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Enveloped viruses, including retroviruses, utilize the host cell's ESCRT pathway for viral budding.
  • Analyzing the ESCRT-mediated budding process can be complex, particularly for viruses like HIV-1 that recruit multiple ESCRT factors.

Purpose of the Study:

  • To investigate the specific ESCRT factor requirements for Equine Infectious Anemia Virus (EIAV) budding.
  • To establish EIAV as a model system for studying lentivirus assembly and ESCRT-mediated budding.

Main Methods:

  • Utilized siRNA depletion of endogenous ESCRT proteins in EIAV-infected cells.
  • Performed rescue experiments using siRNA-resistant wild-type and mutant ESCRT constructs.
  • Analyzed the impact of specific protein interaction-disrupting mutations on EIAV budding.

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Main Results:

  • EIAV budding requires the ESCRT proteins ALIX, CHMP4B, CHMP2A, and VPS4A/B.
  • Disruption of interactions between ALIX:CHMP4B, CHMP4B:CHMP2A, and CHMP2A:VPS4A/B inhibited EIAV budding.
  • Depletion of CHMP4B resulted in the formation of aberrant, multi-lobed, and tubular EIAV virions.

Conclusions:

  • EIAV budding is dependent on a defined ESCRT protein network: Gag-ALIX-CHMP4B-CHMP2A-VPS4.
  • CHMP4B plays a crucial role in regulating Gag polymerization and/or processing for timely ESCRT assembly and membrane fission.
  • EIAV serves as a simplified model for dissecting lentivirus assembly and ESCRT-mediated budding mechanisms.