Loss of CD4 membrane expression and CD4 mRNA during acute human immunodeficiency virus replication.
Loss of CD4 membrane expression and CD4 mRNA during acute human immunodeficiency virus replication.
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DOI：
10.1084/jem.168.6.1953
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发表时间：
1988-12-01
影响因子：
15.3
通讯作者：
KLATZMANN, D
中科院分区：
文献类型：
--
作者：
SALMON, P;OLIVIER, R;RIVIERE, Y;BRISSON, E;GLUCKMAN, JC;KIENY, MP;MONTAGNIER, L;KLATZMANN, D
使用单克隆抗体和基因组探针的CD 4分子，HIV受体，我们证明，HIV复制诱导其功能性受体从细胞表面的消失，通过两种不同的机制。首先，在表达到细胞表面后，HIV包膜gp 110将与CD 4复合，有效地掩蔽病毒用于结合其受体的CD 4表位。这种现象发生在每个感染细胞的表面上，并不是由于可溶性gp 110的释放;表达突变的HIV env基因的重组HIV/牛痘病毒的感染诱导了类似的gp/CD 4复合物的形成，该突变的HIV env基因旨在防止gp 110从细胞表面释放。其次，病毒复制诱导CD 4 mRNA转录物的急剧和快速损失，阻止新的CD 4分子合成。这两种受体调节机制可能是为了避免复制病毒的细胞再次感染，以及产生更具感染性的颗粒。这些结果表明，经典的病毒干扰记录其他逆转录病毒可能不仅是由于受体/包膜相互作用，但也可能取决于受体基因的表达。
Using mAbs and genomic probe to the CD4 molecule, the HIV receptor, we demonstrated that HIV replication induces the disappearance of its functional receptor from the cell surface by two distinct mechanisms. First, after being expressed onto the cell surface, HIV envelope gp110 will complex CD4, efficiently masking the CD4 epitope used by the virus to bind its receptor. This phenomenon occurs on the surface of each infected cell and is not due to the release of soluble gp110; infection with recombinant HIV/vaccinia viruses expressing a mutated HIV env gene designed to prevent gp110 release from the cell surface induces a similar gp/CD4 complexes formation. Second, virus replication induces a dramatic and rapid loss of CD4 mRNA transcripts, preventing new CD4 molecules from being synthesized. These two mechanisms of receptor modulation could have been developed to avoid reinfection of cells replicating the virus as well as to produce more infectious particles. These results suggest that the classical virus interference documented for other retroviruses might not only be due to receptor/envelope interaction, but might also depend on receptor gene expression.
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