Tremblay M, Meloche S, Sekaly R P, Wainberg M A
Lady Davis Institute, Jewish General Hospital, Montreal, Quebec, Canada.
J Exp Med. 1990 May 1;171(5):1791-6. doi: 10.1084/jem.171.5.1791.
Although the CD4 glycoprotein is the primary receptor for HIV-1, recent reports have suggested that other molecules might be involved in the enhancement of HIV-1 infection. We investigated the possible role of the complement receptor 2 in enhancement of HIV-1 infection in CD4+ EBV-containing B cells by infecting such cells in the presence of sera from HIV sero-positive donors, with or without added human complement. A marked increase in production of viral p24 and infectious progeny virus was observed only when infection had been carried out in the presence of human complement. The addition of mAb to the human complement receptor 2 completely inhibited this enhancement. This mechanism was CD4 dependent, suggesting a cooperative effect between these two ligands in the potentiation of viral entry.
尽管CD4糖蛋白是HIV-1的主要受体,但最近的报告表明其他分子可能参与了HIV-1感染的增强。我们通过在有或没有添加人补体的情况下,用来自HIV血清阳性供体的血清感染CD4⁺含EBV的B细胞,研究了补体受体2在增强HIV-1感染中的可能作用。仅当在人补体存在下进行感染时,才观察到病毒p24和感染性子代病毒产生的显著增加。向人补体受体2添加单克隆抗体完全抑制了这种增强作用。这种机制依赖于CD4,表明这两种配体在增强病毒进入方面具有协同作用。