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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

Insights

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.
  • 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.

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