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2009-11-18Zeitschriftenartikel DOI: 10.1099/vir.0.016022-0
Deletion of the rat cytomegalovirus immediate-early 1 gene results in a virus capable of establishing latency, but with lower levels of acute virus replication and latency that compromise reactivation efficiency.
dc.contributor.authorSandford, Gordon R.
dc.contributor.authorSchumacher, Uwe
dc.contributor.authorEttinger, Jakob
dc.contributor.authorBrune, Wolfram
dc.contributor.authorHayward, Gary S.
dc.contributor.authorBurns, William H.
dc.contributor.authorVoigt, Sebastian
dc.date.accessioned2018-05-07T14:12:53Z
dc.date.available2018-05-07T14:12:53Z
dc.date.created2010-11-18
dc.date.issued2009-11-18none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/recS09LCwtBkA/PDF/21DhZnCVDJdbY.pdf
dc.identifier.urihttp://edoc.rki.de/176904/748
dc.description.abstractThe IE1 and IE2 proteins encoded by the major immediate-early (MIE) transcription unit of cytomegaloviruses are thought to play key roles in the switch between latent and lytic cycle infection. Whilst IE2 is essential for triggering the lytic cycle, the exact roles of IE1 have not been resolved. An MIE-exon 4 deleted rat cytomegalovirus ({Delta}IE1) failed to synthesize the IE1 protein and did not disperse promyelocytic leukemia bodies (PML) early post-infection, but it was still capable of normal replication in fibroblast cell culture. However, {Delta}IE1 had diminished ability to infect salivary glands persistently in vivo and to reactivate from spleen explant cultures ex vivo. Quantitation of viral genomes in spleens of infected animals revealed a reduced amount of {Delta}IE1 virus produced during acute infection, suggesting a role for IE1 as a regulator in establishing a chronic or persistent infection, rather than in more directly influencing the latency or reactivation processes.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subjectAnimalseng
dc.subjectDNAeng
dc.subjectVirulenceeng
dc.subjectCellseng
dc.subjectCulturedeng
dc.subjectVirus Replicationeng
dc.subjectViral/geneticseng
dc.subjectMuromegalovirus/geneticseng
dc.subjectRatseng
dc.subjectVirus Activationeng
dc.subjectFibroblasts/virologyeng
dc.subjectHerpesviridae Infections/virologyeng
dc.subjectImmediate-Early Proteins/geneticseng
dc.subjectMuromegalovirus/physiologyeng
dc.subjectSalivary Glands/virologyeng
dc.subjectSequence Deletioneng
dc.subjectSpleen/virologyeng
dc.subjectTrans-Activators/geneticseng
dc.subjectVirus Latencyeng
dc.subject.ddc610 Medizin
dc.titleDeletion of the rat cytomegalovirus immediate-early 1 gene results in a virus capable of establishing latency, but with lower levels of acute virus replication and latency that compromise reactivation efficiency.
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10011475
dc.identifier.doi10.1099/vir.0.016022-0
dc.identifier.doihttp://dx.doi.org/10.25646/673
local.edoc.container-titleJournal of General Virology
local.edoc.container-textThis is an author manuscript that has been accepted for publication in Microbiology, copyright Society for General Microbiology, but has not been copy-edited, formatted or proofed. Cite this article as appearing in Microbiology. This version of the manuscript may not be duplicated or reproduced, other than for personal use or within the rule of ‘Fair Use of Copyrighted Materials’ (section 17, Title 17, US Code), without permission from the copyright owner, Society for General Microbiology. The Society for General Microbiology disclaims any responsibility or liability for errors or omissions in this version of the manuscript or in any version derived from it by any other parties. The final copy-edited, published article, which is the version of record, can be found at http://mic.sgmjournals.org, and is freely available without a subscription 12 months after publication.
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://vir.sgmjournals.org/cgi/content/abstract/vir.0.016022-0v1
local.edoc.container-publisher-nameSociety for General Microbiology
local.edoc.container-volume91
local.edoc.container-issue3
local.edoc.container-year2010

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