Vaccinia virus replication is independent of cellular HSP72 expression which is induced during virus infection

Sedger, L; Ramshaw, I; Condie, A; Medveczky, J; Braithwaite, A; Ruby, J

Vaccinia virus replication is independent of cellular HSP72 expression which is induced during virus infection

Sedger, L

Ramshaw, I Condie, A Medveczky, J Braithwaite, A Ruby, J

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Publication Type:: Journal Article
Citation:: Virology, 1996, 225 (2), pp. 423 - 427
Issue Date:: 1996-11-15

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Field	Value	Language
dc.contributor.author	Sedger, L https://orcid.org/0000-0003-1009-5683	en_US
dc.contributor.author	Ramshaw, I	en_US
dc.contributor.author	Condie, A	en_US
dc.contributor.author	Medveczky, J	en_US
dc.contributor.author	Braithwaite, A	en_US
dc.contributor.author	Ruby, J	en_US
dc.date.issued	1996-11-15	en_US
dc.identifier.citation	Virology, 1996, 225 (2), pp. 423 - 427	en_US
dc.identifier.issn	0042-6822	en_US
dc.identifier.uri	http://hdl.handle.net/10453/8722
dc.description.abstract	HSP72 is dramatically induced in the ovaries of vaccinia virus (VV)-infected mice and associates with VV proteins. In order to Investigate the role of HSP72 during vaccinia virus replication, we have constructed a recombinant vaccinia virus encoding the major inducible cellular HSP72 (VV-HSP72+) and examined the replication characteristics of this virus. VV-HSP72+ exhibited growth kinetics identical to and peak titers very similar to those of control viruses, both in vitro and in vivo. In particular, replication of VV-HSP72+ was identical to that of control viruses in the HSP72-negative cell line Y3.Ag.1.2.3, and overexpression of HSP72 had no effect on the virulence of VV infection in normal or immunocompromised mice. We conclude that while W infection results in the induction of the major inducible 72-kDa HSP, VV replication proceeds normally in the absence of this protein. It is unclear whether another celluar chaperone is required to facilitate virus replication in place of HSP72 in Y3.Ag.1.2.3 cells or whether HSP expression plays no role in virus replication, but is simply a component of the generalized stress response to virus infection.	en_US
dc.relation.ispartof	Virology	en_US
dc.relation.isbasedon	10.1006/viro.1996.0619	en_US
dc.subject.classification	Virology	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice	en_US
dc.subject.mesh	Vaccinia virus	en_US
dc.subject.mesh	Vaccinia	en_US
dc.subject.mesh	Heat-Shock Proteins	en_US
dc.subject.mesh	Virus Replication	en_US
dc.subject.mesh	Female	en_US
dc.title	Vaccinia virus replication is independent of cellular HSP72 expression which is induced during virus infection	en_US
dc.type	Journal Article
utslib.citation.volume	2	en_US
utslib.citation.volume	225	en_US
utslib.for	060103 Cell Development, Proliferation and Death	en_US
utslib.for	060506 Virology	en_US
utslib.for	06 Biological Sciences	en_US
utslib.for	07 Agricultural and Veterinary Sciences	en_US
utslib.for	11 Medical and Health Sciences	en_US
dc.location.activity	ISI:A1996VV42100021	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	closed_access
pubs.issue	2	en_US
pubs.publication-status	Published	en_US
pubs.volume	225	en_US

Abstract:

HSP72 is dramatically induced in the ovaries of vaccinia virus (VV)-infected mice and associates with VV proteins. In order to Investigate the role of HSP72 during vaccinia virus replication, we have constructed a recombinant vaccinia virus encoding the major inducible cellular HSP72 (VV-HSP72+) and examined the replication characteristics of this virus. VV-HSP72+ exhibited growth kinetics identical to and peak titers very similar to those of control viruses, both in vitro and in vivo. In particular, replication of VV-HSP72+ was identical to that of control viruses in the HSP72-negative cell line Y3.Ag.1.2.3, and overexpression of HSP72 had no effect on the virulence of VV infection in normal or immunocompromised mice. We conclude that while W infection results in the induction of the major inducible 72-kDa HSP, VV replication proceeds normally in the absence of this protein. It is unclear whether another celluar chaperone is required to facilitate virus replication in place of HSP72 in Y3.Ag.1.2.3 cells or whether HSP expression plays no role in virus replication, but is simply a component of the generalized stress response to virus infection.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/8722