Objective To explore the mechanism of latent human immunodeficiency ciency virus type 1 (HIV-1) infection is unclear, especially in dendritic cells (DC).We hypothesized that DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) binds with HIV-1 may activate HIV-1 provirus.Methods We generated a model by transfecting 293T cells with a DC-SIGN expression plasmid and a HIV-1 5'long terminal repeat (LTR) reporter plasmid, and then stimulated the 293T cells with HIV-1 gp120 protein, wild-type HIV-1 and VSV-G-pNL4.3 pseudotype virus ( without gp120 protein).CEM-Bru cells were transfected with the DC-SIGN expression plasmid and stimulated by HIV-1 gp120 protein.Then HIV-1 replication was detected.The involvement of the ERK, p38 and NF-κB pathways signaling in this response were determined by inhibiting the pathways specifically and detecting the phosphorylation of the signaling kinase.Results The HIV-1 5'LTR was reactivated by HIV-1 gp120 in DC-SIGN-expressing 293T cells.After HIV-1 gp120 protein stimulation of the mold of CEM-Bru cells, the increasing expression of HIV-1 Tat mRNA and HIV-1 p24,which implies early and late HIV-1 provirus replication was reactivated by the HIV-1 gp120/DC-SIGN stimulation.HIV-1 gp120/DC-SIGN stimulation reactivates latent HIV-1 provirus via the NF-κB signal pathway.Conclusion HIV-1 gp120/DC-SIGN stimulation reactivates latent HIV-1 provirus via the NF-κB signal pathway.%目的：研究HIV-1 gp120蛋白与DC-SIGN结合对HIV-1前病毒的活化作用及其信号通路机制。方法将DC-SIGN表达质粒和HIV-15’末端重复序列（5’LTR）报告质粒转染293T细胞，以HIV-1 gp120蛋白、野生型HIV-1、VSV-G-pNL4.3假病毒分别刺激，检测HIV-15’LTR的活性。慢性感染HIV-1的CEM-Bru 细胞转染DC-SIGN表达质粒，以HIV-1 gp120蛋白刺激，检测HIV-1 Tat mRNA和HIV-1 p24蛋白表达水平。特异性抑制ERK、P38和NF-κB信号通路，再用gp120刺激DC-SIGN（＋） CEM-Bru 细胞，检测HIV-1前病毒的活化。结果在DC-SIGN（＋）293T细胞中，HIV-15'LTR可以被HIV-1 gp120激活。 HIV-1 gp120蛋白及DC-SIGN刺激DC-SIGN（＋） CEM-Bru后，HIV-1 Tat mRNA和HIV-1 p24蛋白表达水平明显升高，提示其早期和晚期HIV-1前病毒复制，用抗体阻断DC-SIGN可抑制潜伏HIV-1活化。 HIV-1 gp120／DC-SIGN 通过NF-κB信号通路在激活潜伏HIV-1前病毒。结论 HIV-1 gp120可通过结合DC-SIGN激活NF-κB信号通路介导HIV-1前病毒活化。
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