Legendre C, Gras G, Krzysiek R, Galanaud P, Richard Y, Dormont D
Service de Neurovirologie, CE-FAR, DSV/DRM/SNV, IPSC, Fontenay aux Roses, France.
FEBS Lett. 1996 Mar 4;381(3):227-32. doi: 10.1016/0014-5793(96)00040-3.
Using our in vitro model of normal B cell infection that functions with low doses of HIV but requires virus opsonization by seropositive patient serum, and complement, we analyzed what receptors allowed virus entry. Here, we show that HIV infection of B cells occurs through 2 major receptors: the CD4 antigen and the CR1/CR2 complex. These 2 pathways work independently since a complete inhibition of virus entry requires both CD4 and CD21/CD35 blockade on CD4dim tonsillar B cells whereas only the latter is critical on CD4-negative B cells.
利用我们的正常B细胞感染体外模型，该模型在低剂量HIV作用下发挥功能，但需要血清反应阳性患者血清和补体对病毒进行调理，我们分析了哪些受体允许病毒进入。在这里，我们表明B细胞的HIV感染通过两种主要受体发生：CD4抗原和CR1/CR2复合体。这两条途径独立起作用，因为对CD4dim扁桃体B细胞而言，要完全抑制病毒进入需要同时阻断CD4和CD21/CD35，而对CD4阴性B细胞而言，只有后者至关重要。
