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2017-02-02Zeitschriftenartikel DOI: 10.1038/ncomms14321
Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein
dc.contributor.authorKrishna, B. A.
dc.contributor.authorSpiess, K.
dc.contributor.authorPoole, E. L.
dc.contributor.authorLau, B.
dc.contributor.authorVoigt, Sebastian
dc.contributor.authorKledal, T. N.
dc.contributor.authorRosenkilde, M. M.
dc.contributor.authorSinclair, J. H.
dc.date.accessioned2018-05-07T19:45:25Z
dc.date.available2018-05-07T19:45:25Z
dc.date.created2017-02-17
dc.date.issued2017-02-02none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/renlPHVYMXoU/PDF/22cTtO8P9Zw.pdf
dc.identifier.urihttp://edoc.rki.de/176904/2554
dc.description.abstractReactivation of human cytomegalovirus (HCMV) in transplant recipients can cause life-threatening disease. Consequently, for transplant recipients, killing latently infected cells could have far-reaching clinical benefits. In vivo, myeloid cells and their progenitors are an important site of HCMV latency, and one viral gene expressed by latently infected myeloid cells is US28. This viral gene encodes a cell surface G protein-coupled receptor (GPCR) that binds chemokines, triggering its endocytosis. We show that the expression of US28 on the surface of latently infected cells allows monocytes and their progenitor CD34+ cells to be targeted and killed by F49A-FTP, a highly specific fusion toxin protein that binds this viral GPCR. As expected, this specific targeting of latently infected cells by F49A-FTP also robustly reduces virus reactivation in vitro. Consequently, such specific fusion toxin proteins could form the basis of a therapeutic strategy for eliminating latently infected cells before haematopoietic stem cell transplantation.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subject.ddc610 Medizin
dc.titleTargeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10051260
dc.identifier.doi10.1038/ncomms14321
dc.identifier.doihttp://dx.doi.org/10.25646/2479
local.edoc.container-titleNature Communications
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://www.nature.com/articles/ncomms14321
local.edoc.container-publisher-nameNature Publishing Group
local.edoc.container-volume8
local.edoc.container-issue14321
local.edoc.container-year2017

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