Partial Functional Complementation between Human and Mouse Cytomegalovirus Chemokine Receptor Homologues
Partial Functional Complementation between Human and Mouse Cytomegalovirus Chemokine Receptor Homologues
复制标题
DOI：
10.1128/jvi.02113-10
复制
发表时间：
2011-06-01
影响因子：
5.4
通讯作者：
Davis-Poynter, Nicholas
中科院分区：
文献类型：
--
作者：
Farrell, Helen E.;Abraham, Alexander M.;Davis-Poynter, Nicholas
人巨细胞病毒(CMV)蛋白US28和UL33与趋化因子受体(CKRs)同源。敲除小鼠CMV M33蛋白(UL33同源物)导致唾液腺感染/复制显著减弱，并降低组织外植体的重新激活效率。M33介导的G蛋白偶联信号对唾液腺的表型至关重要。在这份报告中，我们证明了US28和UL33(在较小程度上)恢复了组织外植体的重新激活，并部分恢复了唾液腺的复制(与信号缺陷的M33突变体相比)。这些研究为评价针对人巨细胞病毒CKRs的治疗提供了一种新的小动物模型。
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.