Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein

Research output: Contribution to journal › Journal article › Research › peer-review

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Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein. / Krishna, B. A.; Spiess, K.; Poole, E. L.; Lau, B.; Voigt, S.; Kledal, Thomas N; Rosenkilde, M. M.; Sinclair, J. H.

In: Nature Communications, Vol. 8, 14321, 02.02.2017.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Krishna, BA, Spiess, K, Poole, EL, Lau, B, Voigt, S, Kledal, TN, Rosenkilde, MM & Sinclair, JH 2017, 'Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein', Nature Communications, vol. 8, 14321. https://doi.org/10.1038/ncomms14321

APA

Krishna, B. A., Spiess, K., Poole, E. L., Lau, B., Voigt, S., Kledal, T. N., Rosenkilde, M. M., & Sinclair, J. H. (2017). Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein. Nature Communications, 8, [14321]. https://doi.org/10.1038/ncomms14321

Vancouver

Krishna BA, Spiess K, Poole EL, Lau B, Voigt S, Kledal TN et al. Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein. Nature Communications. 2017 Feb 2;8. 14321. https://doi.org/10.1038/ncomms14321

Author

Krishna, B. A. ; Spiess, K. ; Poole, E. L. ; Lau, B. ; Voigt, S. ; Kledal, Thomas N ; Rosenkilde, M. M. ; Sinclair, J. H. / Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein. In: Nature Communications. 2017 ; Vol. 8.

Bibtex

@article{4415068b5f9a4053a264162225357b34,
title = "Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein",
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.",
author = "Krishna, {B. A.} and K. Spiess and Poole, {E. L.} and B. Lau and S. Voigt and Kledal, {Thomas N} and Rosenkilde, {M. M.} and Sinclair, {J. H.}",
year = "2017",
month = feb,
day = "2",
doi = "10.1038/ncomms14321",
language = "English",
volume = "8",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein

AU - Krishna, B. A.

AU - Spiess, K.

AU - Poole, E. L.

AU - Lau, B.

AU - Voigt, S.

AU - Kledal, Thomas N

AU - Rosenkilde, M. M.

AU - Sinclair, J. H.

PY - 2017/2/2

Y1 - 2017/2/2

N2 - 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.

AB - 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.

U2 - 10.1038/ncomms14321

DO - 10.1038/ncomms14321

M3 - Journal article

C2 - 28148951

VL - 8

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 14321

ER -

ID: 173562730