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Related Experiment Videos

Retroviruses have differing requirements for proteasome function in the budding process.

David E Ott1, Lori V Coren, Raymond C Sowder

  • 1AIDS Vaccine Program, SAIC-Frederick, Inc., National Cancer Institute at Frederick, Frederick, Maryland 21702-1201, USA. ott@ncifcrf.gov

Journal of Virology
|March 1, 2003
PubMed
Summary
This summary is machine-generated.

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Proteasome inhibitors reduce budding for many retroviruses, including those with cytoplasmic assembly. However, some viruses like MMTV are unaffected, indicating complex interactions with the ubiquitination system.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Proteasome inhibitors are known to impede the budding of certain retroviruses, such as human immunodeficiency virus type 1 (HIV-1).
  • The precise mechanisms and viral targets affected by proteasome inhibitors during retroviral budding remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of proteasome inhibitors on the budding of diverse retroviruses with varying Gag organization, late (L) domain usage, and assembly sites.
  • To determine if proteasome inhibition affects viruses that assemble in the cytoplasm.

Main Methods:

  • Treatment of various cell lines with proteasome inhibitors.
  • Analysis of retroviral particle budding from treated cells.
  • Examination of viral Gag-ubiquitin conjugates in viral particles.

Related Experiment Videos

  • Assessment of proteasome and ubiquitination system activity via protein analysis.

    • Main Results:

    • Proteasome inhibition decreased budding of murine leukemia virus and Mason-Pfizer monkey virus, both utilizing a PPPY L domain.
    • Budding of mouse mammary tumor virus (MMTV), with an unknown L domain, was unaffected by proteasome inhibitors.
    • Gag-ubiquitin conjugates were detected in MMTV particles, suggesting ubiquitination system involvement.
    • Proteasome inhibitors effectively inactivated proteasomes and inhibited the ubiquitination system in treated cells.

    Conclusions:

    • Proteasome inhibitors reduce budding of retroviruses employing PPPY- or PTAP-based L domains, irrespective of their assembly site or Gag ubiquitination status.
    • The effect of proteasome inhibitors on viral budding is virus-specific and may not universally apply to all retroviruses, even those with cytoplasmic assembly.