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Related Experiment Videos

Retrovirus budding.

Eiji Morita1, Wesley I Sundquist

  • 1Department of Biochemistry, University of Utah, Salt Lake City, UT 84132, USA. moritae@biochem.utah.edu

Annual Review of Cell and Developmental Biology
|October 12, 2004
PubMed
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Retroviruses like HIV hijack cell machinery for budding and infection. They exploit multivesicular body pathways to spread, either directly or via exosomes, enhancing host cell infection.

Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Human immunodeficiency virus (HIV) and other retroviruses infect cells by budding.
  • Retroviruses utilize cellular pathways for vesicle formation, specifically multivesicular bodies (MVBs).

Purpose of the Study:

  • To understand how retroviruses, including HIV-1, hijack cellular MVB biogenesis pathways for viral release.
  • To elucidate the mechanisms of viral budding and cell-to-cell transmission.

Main Methods:

  • Investigated the role of cellular proteins in MVB biogenesis and HIV-1 budding.
  • Developed a working model for the sequential recruitment of proteins during MVB vesicle formation.

Main Results:

  • Identified 25 human proteins essential for MVB biogenesis and HIV-1 budding.

Related Experiment Videos

  • Demonstrated that retroviruses can bud from the plasma membrane or MVB compartments.
  • Showed that viruses can be released directionally into virological synapses.

    • Conclusions:

    • Retroviruses have evolved sophisticated mechanisms to usurp cellular pathways for efficient release and infection.
    • Viral budding can occur via direct release from the plasma membrane or through the exosome pathway via MVBs.
    • Virological synapses facilitate directional virus release, optimizing new host cell infection.