dc.contributor.author
Krishna, B. A.
dc.contributor.author
Spiess, K.
dc.contributor.author
Poole, E. L.
dc.contributor.author
Lau, B.
dc.contributor.author
Voigt, S.
dc.contributor.author
Kledal, T. N.
dc.contributor.author
Rosenkilde, M. M.
dc.contributor.author
Sinclair, J. H.
dc.date.accessioned
2018-06-08T10:36:38Z
dc.date.available
2017-03-22T11:05:10.403Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/20747
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-24046
dc.description.abstract
Reactivation 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.
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::615 Pharmakologie, Therapeutik
dc.title
Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin
protein
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Nature Communications. - 8 (2017), Artikel Nr. 14321
dcterms.bibliographicCitation.doi
10.1038/ncomms14321
dcterms.bibliographicCitation.url
http://www.nature.com/articles/ncomms14321
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000026691
refubium.note.author
Der Artikel wurde in einer reinen Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000007939
dcterms.accessRights.openaire
open access