CC趋化因子通过阻断CC趋化因子受体5（CCR5）嗜性的人类免疫缺陷病毒1在人类淋巴组织中的复制
Blockade of CC chemokine receptor 5 (CCR5)-tropic human immunodeficiency virus-1 replication in human lymphoid tissue by CC chemokines.
作者信息
Margolis L B, Glushakova S, Grivel J C, Murphy P M
机构信息
Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
出版信息
J Clin Invest. 1998 May 1;101(9):1876-80. doi: 10.1172/JCI2015.
Abstract
The CC chemokines MIP-1alpha, MIP-1beta, and RANTES suppress replication of certain HIV-1 strains in cultured PBMC and T cell lines by blocking interaction of gp120 with CC chemokine receptor 5 (CCR5). However, the same chemokines can enhance HIV-1 replication in cultured macrophages. The net effect of chemokines on HIV-1 infection in intact lymphoid tissue, the major reservoir of HIV-1 in vivo, is unknown and unpredictable since the tissue contains both T lymphocytes and macrophages. Here we show that exogenous MIP-1alpha, MIP-1beta, and RANTES markedly suppressed replication of CCR5-tropic HIV-1 strains in blocks of human lymphoid tissue infected ex vivo. Moreover, endogenous MIP-1alpha, MIP-1beta, and RANTES were upregulated in tissues infected ex vivo with CXC chemokine receptor 4-tropic but not CCR5-tropic HIV-1. Such an upregulation may contribute to the virus phenotype shift in the course of HIV disease in vivo.
摘要
CC趋化因子MIP-1α、MIP-1β和RANTES通过阻断gp120与CC趋化因子受体5（CCR5）的相互作用，抑制某些HIV-1毒株在培养的外周血单核细胞（PBMC）和T细胞系中的复制。然而，相同的趋化因子可增强HIV-1在培养的巨噬细胞中的复制。趋化因子对完整淋巴组织（体内HIV-1的主要储存库）中HIV-1感染的净效应尚不清楚且无法预测，因为该组织同时含有T淋巴细胞和巨噬细胞。在此我们表明，外源性MIP-1α、MIP-1β和RANTES可显著抑制离体感染的人淋巴组织块中CCR5嗜性HIV-1毒株的复制。此外，在用CXC趋化因子受体4嗜性而非CCR5嗜性HIV-1离体感染的组织中，内源性MIP-1α、MIP-1β和RANTES上调。这种上调可能在体内HIV疾病进程中促成病毒表型转变。
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