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Downregulation of protein disulfide isomerase inhibits infection by the mouse polyomavirus

Joanna Gilbert1, Wu Ou, Jonathan Silver

  • 1Department of Pathology, NRB-939I, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.

Journal of Virology
|August 25, 2006
PubMed

Insights

Mouse polyomavirus infection requires protein disulfide isomerase (PDI). Reducing PDI levels in HeLa cells inhibits viral infectibility by trapping the virus in the endoplasmic reticulum (ER), preventing its exit.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Protein disulfide isomerase (PDI) is a crucial enzyme in the endoplasmic reticulum (ER) involved in protein folding and disulfide bond formation.
  • Viral entry and replication are complex processes that often involve host cell machinery, including the ER.

Purpose of the Study:

  • To investigate the role of protein disulfide isomerase (PDI) in the early stages of mouse polyomavirus infection.
  • To determine if PDI is essential for viral infectibility and replication.

Main Methods:

  • Utilized HeLa cells with stable small interfering RNA (siRNA) mediated downregulation of PDI.
  • Assessed viral infectibility by measuring nuclear T antigen expression.
  • Restored PDI expression using plasmid transfection.
  • Employed deconvolution microscopy with fluorescently labeled virus and cellular markers to track viral localization.

Main Results:

  • PDI downregulation significantly reduced mouse polyomavirus infectibility in a dose-dependent manner.
  • Restoration of PDI expression rescued viral infectibility, while a catalytically inactive mutant did not.
  • Virus successfully reached the ER in PDI-depleted cells but failed to exit the ER.
  • Simian virus 40 infection remained unaffected by PDI downregulation.

Conclusions:

  • Protein disulfide isomerase (PDI) plays a critical role in the post-ER trafficking or disassembly of mouse polyomavirus.
  • The mechanism of inhibition involves the retention of the virus within the ER, suggesting a specific interaction between PDI and the virus.
  • Structural differences between mouse polyomavirus and Simian virus 40 may account for the differential sensitivity to PDI levels.

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