1型人类免疫缺陷病毒进入抑制剂是否需要靶向多个共受体？
Will multiple coreceptors need to be targeted by inhibitors of human immunodeficiency virus type 1 entry?
作者信息
Zhang Y J, Moore J P
机构信息
Aaron Diamond AIDS Research Center, The Rockefeller University, New York, New York, USA.
出版信息
J Virol. 1999 Apr;73(4):3443-8. doi: 10.1128/JVI.73.4.3443-3448.1999.
Abstract
Despite being able to use the Bonzo coreceptor as efficiently as CCR5 in transfected cells, pediatric human immunodeficiency virus type 1 isolate P6 was unable to replicate in peripheral blood mononuclear cells (PBMC) lacking the CCR5 receptor. Furthermore, its replication in wild-type PBMC was completely inhibited by inhibitors of CCR5-mediated entry. Similarly, maternal isolate M6 could use CCR5, CXCR4, Bonzo, and other coreceptors in transfected cells but was completely sensitive to inhibitors of CCR5- and CXCR4-mediated entry when grown in PBMC. The ability of these viruses to use coreceptors in addition to CCR5 and CXCR4 in vitro was, therefore, irrelevant to their drug sensitivity in primary cells. We argue that CCR5 and CXCR4 should remain the primary targets for antiviral drug development, pending strong evidence to the contrary.
摘要
尽管在转染细胞中，小儿人类免疫缺陷病毒1型分离株P6利用邦佐共受体的效率与利用CCR5的效率一样高，但它无法在缺乏CCR5受体的外周血单核细胞（PBMC）中复制。此外，其在野生型PBMC中的复制被CCR5介导的进入抑制剂完全抑制。同样，母体分离株M6在转染细胞中可以利用CCR5、CXCR4、邦佐和其他共受体，但在PBMC中生长时，它对CCR5和CXCR4介导的进入抑制剂完全敏感。因此，这些病毒在体外除了利用CCR5和CXCR4之外还能利用共受体的能力，与它们在原代细胞中的药物敏感性无关。我们认为，在没有有力反证的情况下，CCR5和CXCR4应仍然是抗病毒药物研发的主要靶点。
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