Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues
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Partial functional complementation between human and mouse cytomegalovirus chemokine receptor homologues. / Farrell, Helen E; Abraham, Alexander M; Cardin, Rhonda D; Sparre-Ulrich, Alexander H; Rosenkilde, Mette M; Spiess, Katja; Jensen, Tine H; Kledal, Thomas N; Davis-Poynter, Nicholas.
I: Journal of Virology, Bind 85, Nr. 12, 06.2011, s. 6091-5.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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
VL - 85
SP - 6091
EP - 6095
JO - Journal of Virology
JF - Journal of Virology
SN - 0022-538X
IS - 12
ER -
ID: 137987172