CXCR4作为1型人类免疫缺陷病毒感染原代巨噬细胞的功能性共受体。
CXCR4 as a functional coreceptor for human immunodeficiency virus type 1 infection of primary macrophages.
作者信息
Simmons G, Reeves J D, McKnight A, Dejucq N, Hibbitts S, Power C A, Aarons E, Schols D, De Clercq E, Proudfoot A E, Clapham P R
机构信息
Section of Virology, Chester Beatty Laboratories, Institute of Cancer Research, London SW3 6JB, United Kingdom.
出版信息
J Virol. 1998 Oct;72(10):8453-7. doi: 10.1128/JVI.72.10.8453-8457.1998.
Abstract
The coreceptors used by primary syncytium-inducing (SI) human immunodeficiency virus type 1 isolates for infection of primary macrophages were investigated. SI strains using only CXCR4 replicated equally well in macrophages with or without CCR5 and were inhibited by several different ligands for CXCR4 including SDF-1 and bicyclam derivative AMD3100. SI strains that used a broad range of coreceptors including CCR3, CCR5, CCR8, CXCR4, and BONZO infected CCR5-deficient macrophages about 10-fold less efficiently than CCR5(+) macrophages. Moreover, AMD3100 blocked infection of CCR5-negative macrophages by these strains. Our results therefore demonstrate that CXCR4, as well as CCR5, is used for infection of primary macrophages but provide no evidence for the use of alternative coreceptors.
摘要
研究了原发性合胞体诱导（SI）1型人类免疫缺陷病毒分离株用于感染原代巨噬细胞的共受体。仅使用CXCR4的SI毒株在有或没有CCR5的巨噬细胞中复制情况相同，并且受到几种不同的CXCR4配体（包括SDF-1和双环胺衍生物AMD3100）的抑制。使用包括CCR3、CCR5、CCR8、CXCR4和BONZO在内的多种共受体的SI毒株感染CCR5缺陷巨噬细胞的效率比CCR5（+）巨噬细胞低约10倍。此外，AMD3100可阻断这些毒株对CCR5阴性巨噬细胞的感染。因此，我们的结果表明，CXCR4以及CCR5可用于原代巨噬细胞的感染，但没有提供使用其他共受体的证据。
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