Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway |
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Authors: | Jian Gong Xi-hui Shen Chao Chen Hui Qiu Rong-ge Yang |
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Institution: | 1. The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China;School of Life Science, Huzhou Teachers College, Huzhou 313000, China 2. The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China |
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Abstract: | The human immunodeficiency virus type 1 (HIV-1) can interact with and exploit the host cellular machinery to replicate and
propagate itself. Numerous studies have shown that the Mitogen-activated protein kinase (MAPK) signal pathway can positively
regulate the replication of HIV-1, but exactly how each MAPK pathway affects HIV-1 infection and replication is not understood.
In this study, we used the Extracellular signal-regulated kinase (ERK) pathway inhibitor, PD98059, the Jun N-terminal kinase
(JNK) pathway inhibitor, SP600125, and the p38 pathway inhibitor, SB203580, to investigate the roles of these pathways in
HIV-1 replication. We found that application of PD98059 results in a strong VSV-G pseudotyped HIV-1NL4-3 luciferase reporter virus and HIV-1NL4-3 virus inhibition activity. In addition, SB203580 and SP600125 also elicited marked VSV-G pseudotyped HIV-1NL4-3 luciferase reporter virus inhibition activity but no HIV-1NL4-3 virus inhibition activity. We also found that SB203580 and SP600125 can enhance the HIV-1 inhibition activity of PD98059
when cells were treated with all three MAPK pathway inhibitors in combination. Finally, we show that HIV-1 virus inhibition
activity of the MAPK pathway inhibitors was the result of the negative regulation of HIV-1 LTR promoter activity. |
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Keywords: | HIV-1 inhibition Mitogen-activated protein kinase(MAPK) Extracellular signal-regulated kinase(ERK) Jun N-terminal kinase(JNK) p38 LTR activation |
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