Halary Franck, Amara Ali, Lortat-Jacob Hugues, Messerle Martin, Delaunay Thierry, Houlès Corinne, Fieschi Franck, Arenzana-Seisdedos Fernando, Moreau Jean François, Déchanet-Merville Julie
Laboratoire d'immunologie, CNRS UMR 5540, Université Bordeaux 2, France.
Immunity. 2002 Nov;17(5):653-64. doi: 10.1016/s1074-7613(02)00447-8.
Cytomegalovirus (CMV) infection is characterized by host immunosuppression and multiorganic involvement. CMV-infected dendritic cells (DC) were recently shown to display reduced immune functions, but their role in virus dissemination is not clear. In this report, we demonstrated that CMV could be captured by DC through binding on DC-SIGN and subsequently transmitted to permissive cells. Moreover, blocking DC-SIGN by specific antibodies inhibited DC infection by primary CMV isolates and expression of DC-SIGN or its homolog DC-SIGNR rendered susceptible cells permissive to CMV infection. We demonstrated that CMV envelope glycoprotein B is a viral ligand for DC-SIGN and DC-SIGNR. These results provide new insights into the molecular interactions contributing to cell infection by CMV and extend DC-SIGN implication in virus propagation.
巨细胞病毒(CMV)感染的特征是宿主免疫抑制和多器官受累。最近研究表明,被CMV感染的树突状细胞(DC)免疫功能降低,但其在病毒传播中的作用尚不清楚。在本报告中,我们证明CMV可通过与DC-SIGN结合被DC捕获,随后传递给易感细胞。此外,用特异性抗体阻断DC-SIGN可抑制原代CMV分离株对DC的感染,而DC-SIGN或其同源物DC-SIGNR的表达可使易感细胞对CMV感染敏感。我们证明CMV包膜糖蛋白B是DC-SIGN和DC-SIGNR的病毒配体。这些结果为CMV导致细胞感染的分子相互作用提供了新见解,并扩展了DC-SIGN在病毒传播中的意义。