An intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) efficiently blocks HIV viral budding.
An intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) efficiently blocks HIV viral budding.
复制标题
细胞间粘附分子 3 (ICAM-3) 抓取非整联蛋白 (DC-SIGN) 可有效阻止 HIV 病毒出芽。
DOI：
10.1096/fj.07-9443com
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Pang,Shen
中科院分区：
文献类型：
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作者：
Wang,Qiuwei;Pang,Shen
在病毒感染、逆转录和翻译后加工阶段有效抑制HIV感染生命周期已得到广泛研究。然而，尚未报道有效抑制HIV组装和出芽。在这里，我们报告了树突状细胞特异性细胞间粘附分子-3（ICAM-3）-抓取非整合素（DC-SIGN）及其相关蛋白DC-SIGNR，有效地阻止了HIV从感染细胞中出芽。DC‐SIGN或DC‐SIGNR与HIV的共转染证明了对宿主细胞病毒产生的95-99.5%抑制。DC-SIGN或DC-SIGNR也可以有效抑制90 - 95%的HIV从感染细胞中产生。DC-SIGN有效地减少了细胞质膜上存在的gp 120的量，并从宿主细胞产生的病毒体中完全剥离gp 120，这表明HIV出芽的阻断是由于DC-SIGN内化了gp 120。王建奎，庞氏S.细胞间粘附分子-3（ICAM-3）-抓取非整合素（DC-SIGN）可有效阻断HIV病毒出芽。FASEB J. 22，1055-1064（2008）
Efficient inhibition of the HIV infection life cycle at the stages of viral infection, reverse transcription, and post‐translational processing has been extensively studied. However, efficient inhibition of HIV assembly and budding has not been reported. Here, we report that dendritic cell‐specific intercellular adhesion molecule‐3 (ICAM‐3) ‐grabbing nonintegrin (DC‐SIGN) and its related protein, DC‐SIGNR, effectively block HIV budding from infected cells. Cotrans‐fection of DC‐SIGN or DC‐SIGNR with HIV demonstrated 95–99.5% inhibition of viral production from host cells. DC‐SIGN or DC‐SIGNR can also effectively inhibit 90 ‐95% of HIV generation from infected cells. DC‐SIGN efficiently reduces the amount of gp120 present on the cell plasma membrane, and completely strips off gp120 from the virions produced by the host cells, suggesting that blockage of HIV budding is due to internalization of gp120 by DC‐SIGN. Wang, Q., Pang, S. An intercellular adhesion molecule‐3 (ICAM‐3) ‐grabbing nonintegrin (DC‐SIGN) efficiently blocks HIV viral budding. FASEB J. 22, 1055–1064 (2008)