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Endoplasmic reticulum chaperone gp96 is essential for infection with vesicular stomatitis virus
Abstract
The envelope glycoprotein of vesicular stomatitis virus (VSV-G) enables viral entry into hosts as distant as insects and vertebrates. Because of its ability to support infection of most, if not all, human cell types VSV-G is used in viral vectors for gene therapy. However, neither the receptor nor any specific host factor for VSV-G has been identified. Here we demonstrate that infection with VSV and innate immunity via Toll-like receptors (TLRs) require a shared component, the endoplasmic reticulum chaperone gp96. Cells without gp96 or with catalytically inactive gp96 do not bind VSV-G. The ubiquitous expression of gp96 is therefore essential for the remarkably broad tropism of VSV-G. Cells deficient in gp96 also lack functional TLRs, which suggests that pathogen-driven pressure for TLR-mediated immunity maintains the broad host range of VSV-G by positively selecting for the ubiquitous expression of gp96.
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Comparison of gp96-knockout and gp96-reconstituted murine pre-B cells found that the cell surface expression of 29 proteins was decreased >3.0 fold in the absence of gp96.
“A comparison of gp96-knockout and gp96-reconstituted murine pre-B cells3,13 found that the cell surface expression of 29 proteins was decreased >3.0 fold in the absence of gp96.”
Western blotting analysis of gp96 from M36 lysates showed a truncated protein at low abundance.
“This corresponds to Western blotting analysis of gp96 from M36 lysates which showed a truncated protein at low abundance.13”
The E4.126 clone was independently derived from 70Z/3 cells by ICR191 mutagenesis and also carries two frameshifting mutations in gp96.
“The E4.126 clone was independently derived from 70Z/3 cells by ICR191 mutagenesis, and also carries two frameshifting mutations in gp96.3,13”
The M36 clone has two frameshift mutations in the ORF of gp96, resulting in production of a truncated nonfunctional protein.
“The resulting M36 clone has two frameshift mutations in the ORF of gp96, resulting in production of a truncated nonfunctional protein.13”
The two frameshifting mutations in the ORF of gp96 in M36 cells explain the loss of wild-type protein.
“The two frameshifting mutations in the ORF of gp96 in M36 cells explain the loss of wild-type protein.13”
Gp96-deficient (M36 and E4.126) cells are resistant to infection by vesicular stomatitis virus (VSV) and viruses pseudotyped with VSV-G.
“Gp96-deficient (M36 and E4.126) cells are resistant to infection by vesicular stomatitis virus (VSV) and viruses pseudotyped with VSV-G13 suggesting that one or more of the extended LDLR family, or indeed other gp96-dependent proteins identified in this analysis may be the receptor for VSV-G.”
One or more of the extended LDLR family, or other gp96-dependent proteins identified in this analysis, may be the receptor for VSV-G.
“Gp96-deficient (M36 and E4.126) cells are resistant to infection by vesicular stomatitis virus (VSV) and viruses pseudotyped with VSV-G13 suggesting that one or more of the extended LDLR family, or indeed other gp96-dependent proteins identified in this analysis may be the receptor for VSV-G.”
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Research works printed but not linked: 30
- JK Rose, MA Whitt, Rhabdoviridae: The Viruses and Their Replication. Fields Virology, eds DM Knipe, PM Howley (Lippincott, Williams, & Williams, Ed 4, Philadelphia) 1, 1221–1244 (2001).
- 10.1016/S0168-1702(02)00026-6 · DOI
- 10.1038/sj.onc.1209042 · DOI
- 10.1073/pnas.90.17.8033 · DOI · Paper page
- 10.2174/1566523054546224 · DOI
- 10.1128/JVI.01864-08 · DOI
- 10.1074/jbc.M008753200 · DOI
- 10.1126/science.1127683 · DOI
- 10.1126/science.1135710 · DOI
- 10.1038/ncb1269 · DOI
- 10.1196/annals.1443.020 · DOI
- 10.1084/jem.189.11.1777 · DOI
- 10.1038/ni1297 · DOI · Paper page
- 10.1084/jem.20071132 · DOI
- 10.1038/ncb1001-891 · DOI · Paper page
- 10.1016/j.immuni.2006.12.005 · DOI · Paper page
- 10.1091/mbc.e07-03-0275 · DOI
- 10.1073/pnas.0706552105 · DOI
- R Krumbach, S Bloor, G Ryzhakov, F Randow, Somatic cell genetics for the study of NF-{kappa}B signaling in innate immunity. Sci Signal 1, pt7 (2008).
- 10.1016/0092-8674(83)90483-X · DOI
- 10.1128/JVI.78.20.10920-10926.2004 · DOI
- 10.1016/S0021-9258(17)43092-4 · DOI
- 10.1073/pnas.83.21.8117 · DOI
- 10.1007/s00249-005-0012-z · DOI
- 10.1128/JVI.79.17.11496-11500.2005 · DOI
- 10.1128/JVI.76.8.3756-3764.2002 · DOI
- 10.1038/nature03571 · DOI
- 10.1007/978-1-4020-4896-8_30 · DOI
- 10.1038/sj.emboj.7601743 · DOI
- 10.1089/10430340252898984 · DOI
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Sorted by citations
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Berger Rentsch, M., & Zimmer, G. (2011) · PLoS ONE · doi:10.1371/journal.pone.0025858 · Cited by 269
Weekes, M. P., Antrobus, R., Talbot, S., Hör, S., Simecek, N., Smith, D. L., Bloor, S., Randow, F., & Lehner, P. J. (2012) · Journal of Proteome Research · doi:10.1021/pr201135e · Cited by 82
Self-citation
Metadata
- Authors
- Bloor, S., Maelfait, J., Krumbach, R., Beyaert, R., & Randow, F.
- Affiliations
- Division of Protein and Nucleic Acid Chemistry, Medical Research Council Laboratory of Molecular Biology, Cambridge CB0 2QH, United Kingdom;
- Unit of Molecular Signal Transduction in Inflammation, Department for Molecular Biomedical Research, Flanders Institute for Biotechnology, B-9052 Ghent, Belgium; and
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-03-29
- Volume
- 107
- Issue
- 15
- Pages
- 6970-6975
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 48
- References
- 0
- Language
- en
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