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The ER-Resident Protein PDZD8 Inhibits Virus Production of West Nile Virus

Shiori Abe1, Akari Sato1, Haruto Eguchi1

  • 1Laboratory of Public Health, Faculty of Veterinary Medicine, Hokkaido University, Hokkaido, Japan.

Microbiology and Immunology
|June 29, 2026
PubMed

Insights

West Nile virus (WNV) infection lowers PDZD8 protein levels, which normally inhibits virus production. This WNV strategy helps the virus assemble and release more efficiently.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • West Nile virus (WNV) alters host cell endoplasmic reticulum (ER) membranes for replication.
  • The precise molecular mechanisms of WNV-induced membrane remodeling are not fully understood.
  • PDZD8 protein facilitates ER-mitochondria contact and lipid transfer, processes involved in membrane dynamics.

Purpose of the Study:

  • To investigate the role of PDZD8 in WNV infection.
  • To elucidate the molecular mechanisms by which WNV interacts with PDZD8 and host membranes.

Main Methods:

  • Analysis of PDZD8 expression levels during WNV infection.
  • Assessment of ER-mitochondria contact sites in infected cells.
  • Evaluation of PDZD8's effect on WNV assembly and release.

Main Results:

  • WNV infection significantly reduced PDZD8 expression.
  • Reduced PDZD8 led to fewer ER-mitochondria contact sites.
  • PDZD8 was found to inhibit WNV particle assembly and release.

Conclusions:

  • WNV suppresses PDZD8 expression to facilitate its own replication.
  • PDZD8 acts as a host factor that restricts WNV production.
  • Targeting PDZD8 could be a potential antiviral strategy against WNV.
Keywords:
ER–mitochondria contactPDZD8West Nile virusmembrane remodelingviral production

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