DC-SIGN-mediated internalization of HIV is required for trans-enhancement of T cell infection

被引:415
作者
Kwon, DS
Gregorio, G
Bitton, N
Hendrickson, WA
Littman, DR [1 ]
机构
[1] NYU, Sch Med, Skirball Inst Biomol Med, Howard Hughes Med Inst, New York, NY 10016 USA
[2] NYU, Sch Med, Skirball Inst Biomol Med, Mol Pathogenesis Program, New York, NY 10016 USA
[3] Columbia Univ Coll Phys & Surg, Dept Biochem & Mol Biophys, Howard Hughes Med Inst, New York, NY 10032 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S1074-7613(02)00259-5
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Fusion of the human immunodeficiency virus (HIV) to the plasma membrane of target cells is mediated by interaction of its envelope glycoprotein, gp120, with CD4 and appropriate chemokine receptors. gp120 additionally binds to DC-SIGN, a C-type lectin expressed on immature dendritic cells. This interaction does not result in viral fusion, but instead contributes to enhanced infection in trans of target cells that express CD4 and chemokine receptors. Here we show that DC-SIGN mediates rapid internalization of intact HIV into a low pH nonlysosomal compartment. Internalized virus retains competence to infect target cells. Removal of the DC-SIGN cytoplasmic tail reduced viral uptake and abrogated the trans-enhancement of T cell infection. We propose that HIV binds to DC-SIGN to gain access to an intracellular compartment that contributes to augmentation or retention of viral infectivity.
引用
收藏
页码:135 / 144
页数:10
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