Kaufman Thomas M, McLinden James H, Xiang Jinhua, Engel Alfred M, Stapleton Jack T
Iowa City VA Medical Center and the University of Iowa, Iowa City, Iowa, USA.
AIDS. 2007 May 11;21(8):1045-8. doi: 10.1097/QAD.0b013e3280f77412.
The addition of GB virus C (GBV-C) E2 protein to cells inhibits HIV replication in vitro, presumably triggered by interactions with a specific cellular receptor. Indirect evidence suggests that CD81 is the GBV-C E2 cellular receptor. We found that E2 binding to cells was not dependent upon human CD81, and that soluble CD81 did not compete with GBV-C E2 for cell binding. GBV-C E2 protein thus does not appear to interact with CD81.
在细胞中添加丙型肝炎病毒(GBV-C)E2蛋白可在体外抑制HIV复制,这可能是由与特定细胞受体的相互作用触发的。间接证据表明,CD81是GBV-C E2的细胞受体。我们发现,E2与细胞的结合不依赖于人类CD81,并且可溶性CD81不能与GBV-C E2竞争细胞结合。因此,GBV-C E2蛋白似乎不与CD81相互作用。