Macrophage tropism of human immunodeficiency virus type 1 and utilization of the CC-CKR5 coreceptor
Macrophage tropism of human immunodeficiency virus type 1 and utilization of the CC-CKR5 coreceptor
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DOI：
10.1128/jvi.71.2.1657-1661.1997
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发表时间：
1997-02-01
影响因子：
5.4
通讯作者：
Stamatatos, L
中科院分区：
文献类型：
--
作者：
ChengMayer, C;Liu, R;Stamatatos, L
最近发现CC-CKR5β趋化因子受体是人类免疫缺陷病毒1型(HIV-1)嗜巨噬细胞分离株进入的主要辅因子，这提出了一个问题，即巨噬细胞的趋化是否是通过利用这种趋化因子受体来决定的。我们观察到，除了A、B和E分支的亲巨噬细胞分离物外，F分支的亲巨噬细胞分离物也利用CC-CKR5分子进入。然而，使用携带嗜T细胞系或嗜巨噬细胞表型重组和突变HTV-1株包膜基因的单轮复制能力报告病毒感染共表达CD4和趋化因子受体的稳定细胞系，我们无法建立巨噬细胞趋化与CC-CKR5趋化因子受体利用之间的严格关联。后者的发现表明，CC-CKR5以外的辅因子是决定进入初级巨噬细胞的决定因素。
The recent identification of the CC-CKR5 beta chemokine receptor as a major cofactor for entry of macrophage-tropic isolates of human immunodeficiency virus type 1 (HIV-1) raises the question of whether macrophage tropism is determined by utilization of this chemokine receptor. We observe that in addition to macrophage-tropic isolates of clades A, B, and E, macrophage-tropic isolates of clade F also utilize the CC-CKR5 molecule for entry. However, using single-round replication-competent reporter viruses carrying the envelope genes of T-cell line-tropic or macrophage-tropic phenotypic recombinant and mutant HTV-1 strains in infection of stable cell lines that coexpress the CD4 and chemokine receptors, we were unable to establish a strict correlation between macrophage tropism and utilization of the CC-CKR5 chemokine receptor. This latter finding suggests that a cofactor other than CC-CKR5 serves to determine entry into primary macrophages.