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Volume 26 Issue 2
April 2011

    Jian Gong, Xi-hui Shen, Chao Chen, Hui Qiu and Rong-ge Yang. Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway*[J]. Virologica Sinica, 2011, 26(2): 114-122. doi: 10.1007/s12250-011-3184-y
    Citation: Jian Gong, Xi-hui Shen, Chao Chen, Hui Qiu, Rong-ge Yang. Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway* .VIROLOGICA SINICA, 2011, 26(2) : 114-122.  http://dx.doi.org/10.1007/s12250-011-3184-y
    shu

    Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway*

    cstr: 32224.14.s12250-011-3184-y
    • 1.

      The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; 2School of Life Science, Huzhou Teachers College, Huzhou 313000, China

    • 通讯作者： Rong-ge Yang, ryang@wh.iov.cn
    • 收稿日期： 2011-01-20
      录用日期： 2011-02-15

    • 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.

    Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway*

    • 1.

      The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China

    • 2.

      School of Life Science, Huzhou Teachers College, Huzhou 313000, China

    • Corresponding author: Rong-ge Yang, ryang@wh.iov.cn
    • Received Date: 20 January 2011
      Accepted Date: 15 February 2011

      Fund Project: Key Projects in the National Science and Technology Pillar Program during the Eleventh Five-Year Plan Period of China 2008ZX10001-002Major Science and Technology Innovation Cross Project of the Chinese Academy of Sciences KSCX1-YW-10

    • 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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      Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway*

        Corresponding author: Rong-ge Yang, ryang@wh.iov.cn
      • 1. The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China
      • 2. School of Life Science, Huzhou Teachers College, Huzhou 313000, China
      • Received Date: 20 January 2011
      • Accepted Date: 15 February 2011
      Fund Project:  Key Projects in the National Science and Technology Pillar Program during the Eleventh Five-Year Plan Period of China 2008ZX10001-002Major Science and Technology Innovation Cross Project of the Chinese Academy of Sciences KSCX1-YW-10

      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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