期刊
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 48, 期 3, 页码 275-281出版社
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gmv138
关键词
HIV-1; DC; DC-SIGN; viral latency; signaling pathways; NF-kappa B
资金
- National Natural Science Foundation of China [81402726]
- Fund for Doctor Discipline Points in Colleges and Universities by Ministry of Education of China [20120101120108]
- Zhejiang Provincial Science and Technology Foundation [2015C33183]
- Zhejiang Medical Science Foundation [2012RCA021]
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases
The reactivation mechanism of latent human immunodeficiency virus type 1 (HIV-1) infection is unclear, especially in dendritic cells (DC). DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) binds with HIV-1 and other pathogens to activate the extracellular regulated protein kinase (ERK) and nuclear factor-kappa B (NF-kappa B) pathways and regulate cytokine expression. We hypothesized that DC-SIGN-induced signaling pathways may activate HIV-1 provirus. To investigate this hypothesis, we generated a model by transfecting 293T cells with a DC-SIGN expression plasmid and an HIV-1 5' long terminal repeat (LTR) reporter plasmid, and then stimulated the 293T cells with HIV-1 gp120 protein, wild-type HIV-1 or VSV-G-pNL4.3 pseudotype virus (without gp120 protein). It was found that the HIV-1 5' LTR was reactivated by HIV-1 gp120 in DC-SIGN-expressing 293T cells. Then the HIV-1 chronically infected CEM-Bru cells were transfected with DC-SIGN expression plasmid and stimulated by HIV-1 gp120 protein. It was found that early and late HIV-1 provirus replication was reactivated by the HIV-1 gp120/DC-SIGN stimulation. We then investigated the involvement of the ERK, p38 mitogen-activated protein kinases and NF-kappa B signaling pathways in HIV-1 gp120/DC-SIGN-induced activation of HIV-1 provirus by inhibiting the pathways specifically. Our results indicated that HIV-1 gp120/DC-SIGN stimulation reactivates latent HIV-1 provirus via the NF-kappa B signal pathway.
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