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Mitochondrial protein p32/HAPB1/gC1qR/C1qbp is required for efficient respiratory syncytial virus production

MengJie Hu1, Hong-Mei Li2, Marie A Bogoyevitch3

  • 1Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia; Cell Signalling Research Laboratories and Bio21 Institute, Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria 3010, Australia.

Biochemical and Biophysical Research Communications
|June 4, 2017
PubMed

Insights

Respiratory syncytial virus (RSV) infection relies on the host mitochondrial protein p32. Reducing p32 levels inhibits RSV replication and virus production, highlighting mitochondria

Area of Science:

  • Virology
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Respiratory syncytial virus (RSV) causes severe respiratory infections in infants and the elderly.
  • Currently, no effective antiviral treatments or vaccines exist for RSV, posing a significant public health challenge.
  • The host cell's role in supporting viral replication is increasingly recognized.

Purpose of the Study:

  • To investigate the function of the host mitochondrial protein p32 (also known as HABP/gC1qR/C1qbp) in the context of RSV infection.
  • To determine if p32 plays a role in viral replication and production.
  • To explore the impact of RSV infection on mitochondrial organization and the localization of p32.

Main Methods:

  • Utilized siRNA knockdown to reduce p32 expression in host cells.
  • Assessed RSV replication and infectious virus production following p32 knockdown.
  • Employed immunostaining and high-resolution confocal microscopy to visualize p32 localization, mitochondrial organization (MitoTracker Red), and cytochrome c distribution.
  • Analyzed changes in mitochondrial morphology and distribution at specific time points post-infection (8 and 18 hours).

Main Results:

  • p32 siRNA knockdown significantly reduced both RSV replication and the production of infectious virus particles.
  • p32 was observed to have distinct mitochondrial localization throughout the course of RSV infection.
  • RSV infection induced significant alterations in mitochondrial organization, including perinuclear compaction and asymmetric distribution of mitochondria.

Conclusions:

  • The host mitochondrial protein p32 is implicated as a key factor supporting RSV virus production.
  • Mitochondria and their organizational dynamics are highlighted as potentially crucial components in the pathogenesis of RSV infection.
  • Targeting host factors like p32 could represent a novel therapeutic strategy against RSV.
Keywords:
Cytochrome cMitochondriaRespiratory syncytial virusp32/HAPB1/gC1qR/C1qbp

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