Moore J P
Aaron Diamond AIDS Research Center, New York University School of Medicine, New York 10016.
J Virol. 1993 Jun;67(6):3656-9. doi: 10.1128/JVI.67.6.3656-3659.1993.
The CDR-3 region of CD4 has been proposed to be involved in the fusion reaction between human immunodeficiency virus type 1 (HIV-1) and CD4+ cells, either at a stage involving virus binding or subsequent to virus binding. Part of the evidence for this has been the observation that monoclonal antibodies (MAbs) to CDR-3 block HIV infection potently without strongly inhibiting the binding of monomeric gp120 to CD4. Here I show that, in a system using oligomeric, virion-bound gp120, a MAb to CDR-3 resembles those to CDR-2 in that it inhibits soluble CD4 binding to virions. Consequently, ternary complexes of MAb-soluble CD4-gp120 cannot be detected with CDR-2 MAbs and are detectable only at a very low level with a CDR-3 MAb, but they clearly form when a control MAb to CD4 domain 4 is used. Although not in direct conflict with previously published data on the role of CDR-3 MAbs in the inhibition of HIV-1 infection, these experiments do not support the hypothesis that the CDR-3 region is specifically involved in virus entry at a postbinding stage.
有人提出，CD4的互补决定区3（CDR-3）参与了1型人类免疫缺陷病毒（HIV-1）与CD4+细胞之间的融合反应，这一过程可能发生在病毒结合阶段，也可能在病毒结合之后。部分证据是观察到针对CDR-3的单克隆抗体（MAb）能有效阻断HIV感染，却不会强烈抑制单体gp120与CD4的结合。在此我表明，在一个使用寡聚的、病毒体结合的gp120的系统中，针对CDR-3的MAb与针对CDR-2的MAb类似，都会抑制可溶性CD4与病毒体的结合。因此，用CDR-2 MAb无法检测到MAb-可溶性CD4-gp120三元复合物，用CDR-3 MAb只能在非常低的水平检测到，但使用针对CD4结构域4的对照MAb时它们明显会形成。尽管这些实验与之前发表的关于CDR-3 MAb在抑制HIV-1感染中作用的数据并不直接冲突，但并不支持CDR-3区域在结合后阶段特异性参与病毒进入的假说。
