Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues

Helen E Farrell; Alexander M Abraham; Rhonda D Cardin; Alexander H Sparre-Ulrich; Mette M Rosenkilde; Katja Spiess; Tine H Jensen; Thomas N Kledal; Nicholas Davis-Poynter

doi:10.1128/JVI.02113-10

Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues

Helen E Farrell, Alexander M Abraham, Rhonda D Cardin, Alexander H Sparre-Ulrich, Mette M Rosenkilde, Katja Spiess, Tine H Jensen, Thomas N Kledal, Nicholas Davis-Poynter

26 Citationer (Scopus)

Abstract

The human cytomegalovirus (CMV) proteins US28 and UL33 are homologous to chemokine receptors (CKRs). Knockout of the mouse CMV M33 protein (UL33 homologue) results in substantial attenuation of salivary gland infection/replication and reduced efficiency of reactivation from tissue explants. M33-mediated G protein-coupled signaling is critical for the salivary gland phenotype. In this report, we demonstrate that US28 and (to a lesser degree) UL33 restore reactivation from tissue explants and partially restore replication in salivary glands (compared to a signaling-deficient M33 mutant). These studies provide a novel small animal model for evaluation of therapies targeting the human CMV CKRs.

Originalsprog	Engelsk
Tidsskrift	Journal of Virology
Vol/bind	85
Udgave nummer	12
Sider (fra-til)	6091-5
Antal sider	5
ISSN	0022-538X
DOI	https://doi.org/10.1128/JVI.02113-10
Status	Udgivet - jun. 2011

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10.1128/JVI.02113-10

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title = "Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues",

abstract = "The human cytomegalovirus (CMV) proteins US28 and UL33 are homologous to chemokine receptors (CKRs). Knockout of the mouse CMV M33 protein (UL33 homologue) results in substantial attenuation of salivary gland infection/replication and reduced efficiency of reactivation from tissue explants. M33-mediated G protein-coupled signaling is critical for the salivary gland phenotype. In this report, we demonstrate that US28 and (to a lesser degree) UL33 restore reactivation from tissue explants and partially restore replication in salivary glands (compared to a signaling-deficient M33 mutant). These studies provide a novel small animal model for evaluation of therapies targeting the human CMV CKRs.",

keywords = "Animals, Cytomegalovirus, Cytomegalovirus Infections, Disease Models, Animal, Female, Herpesviridae Infections, Humans, Mice, Mice, Inbred BALB C, Muromegalovirus, Organ Specificity, Receptors, Chemokine, Salivary Glands, Viral Proteins, Virus Activation, Virus Latency, Virus Replication",

author = "Farrell, {Helen E} and Abraham, {Alexander M} and Cardin, {Rhonda D} and Sparre-Ulrich, {Alexander H} and Rosenkilde, {Mette M} and Katja Spiess and Jensen, {Tine H} and Kledal, {Thomas N} and Nicholas Davis-Poynter",

year = "2011",

month = jun,

doi = "10.1128/JVI.02113-10",

language = "English",

volume = "85",

pages = "6091--5",

journal = "Journal of Virology",

issn = "0022-538X",

publisher = "American Society for Microbiology",

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TY - JOUR

T1 - Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues

AU - Farrell, Helen E

AU - Abraham, Alexander M

AU - Cardin, Rhonda D

AU - Sparre-Ulrich, Alexander H

AU - Rosenkilde, Mette M

AU - Spiess, Katja

AU - Jensen, Tine H

AU - Kledal, Thomas N

AU - Davis-Poynter, Nicholas

PY - 2011/6

Y1 - 2011/6

N2 - The human cytomegalovirus (CMV) proteins US28 and UL33 are homologous to chemokine receptors (CKRs). Knockout of the mouse CMV M33 protein (UL33 homologue) results in substantial attenuation of salivary gland infection/replication and reduced efficiency of reactivation from tissue explants. M33-mediated G protein-coupled signaling is critical for the salivary gland phenotype. In this report, we demonstrate that US28 and (to a lesser degree) UL33 restore reactivation from tissue explants and partially restore replication in salivary glands (compared to a signaling-deficient M33 mutant). These studies provide a novel small animal model for evaluation of therapies targeting the human CMV CKRs.

AB - The human cytomegalovirus (CMV) proteins US28 and UL33 are homologous to chemokine receptors (CKRs). Knockout of the mouse CMV M33 protein (UL33 homologue) results in substantial attenuation of salivary gland infection/replication and reduced efficiency of reactivation from tissue explants. M33-mediated G protein-coupled signaling is critical for the salivary gland phenotype. In this report, we demonstrate that US28 and (to a lesser degree) UL33 restore reactivation from tissue explants and partially restore replication in salivary glands (compared to a signaling-deficient M33 mutant). These studies provide a novel small animal model for evaluation of therapies targeting the human CMV CKRs.

KW - Animals

KW - Cytomegalovirus

KW - Cytomegalovirus Infections

KW - Disease Models, Animal

KW - Female

KW - Herpesviridae Infections

KW - Humans

KW - Mice

KW - Mice, Inbred BALB C

KW - Muromegalovirus

KW - Organ Specificity

KW - Receptors, Chemokine

KW - Salivary Glands

KW - Viral Proteins

KW - Virus Activation

KW - Virus Latency

KW - Virus Replication

U2 - 10.1128/JVI.02113-10

DO - 10.1128/JVI.02113-10

M3 - Journal article

C2 - 21490099

SN - 0022-538X

VL - 85

SP - 6091

EP - 6095

JO - Journal of Virology

JF - Journal of Virology

IS - 12

ER -

Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues

Abstract

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