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

MengJie Hu; Hong-Mei Li; Marie A Bogoyevitch; David A Jans

doi:10.1016/j.bbrc.2017.05.171

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

Biochem Biophys Res Commun. 2017 Aug 5;489(4):460-465. doi: 10.1016/j.bbrc.2017.05.171. Epub 2017 May 30.

Authors

MengJie Hu¹, Hong-Mei Li², Marie A Bogoyevitch³, David A Jans⁴

Affiliations

¹ Nuclear 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.
² Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
³ Cell Signalling Research Laboratories and Bio21 Institute, Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria 3010, Australia.
⁴ Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia. Electronic address: David.Jans@monash.edu.

PMID: 28576489
DOI: 10.1016/j.bbrc.2017.05.171

Abstract

Respiratory syncytial virus (RSV) is a major cause of respiratory infections in infants and the elderly, leading to more deaths than influenza each year, but there is no antiviral or efficacious vaccine currently available. Here we examine the role in infection of the host mitochondrial protein p32 (HABP/gC1qR/C1qbp) for the first time. RSV replication as well as infectious virus production was significantly reduced by p32 siRNA knockdown, consistent with an important role for p32 in RSV infection. p32 showed distinct mitochondrial localization throughout RSV infection, but immunostaining and high resolution confocal imaging for p32 as well as MitoTracker Red and cytochrome c, revealed clear changes in mitochondrial organization in RSV infection, with perinuclear mitochondrial compaction and asymmetric distribution at 8 and 18 h post-infection, respectively. The results implicate p32 as a key host factor for RSV virus production, and bring to light the potential importance of mitochondria in RSV infection.

Keywords: Cytochrome c; Mitochondria; Respiratory syncytial virus; p32/HAPB1/gC1qR/C1qbp.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

A549 Cells
Carrier Proteins / genetics
Carrier Proteins / metabolism*
Humans
Mitochondrial Proteins / genetics
Mitochondrial Proteins / metabolism*
RNA, Small Interfering / genetics
Respiratory Syncytial Viruses / growth & development*
Respiratory Syncytial Viruses / metabolism*
Tumor Cells, Cultured

Substances

C1QBP protein, human
Carrier Proteins
Mitochondrial Proteins
RNA, Small Interfering