Lars Jørgen Østergaard

Role of mitogen-activated protein kinases, nuclear factor-κB, and interferon regulatory factor 3 in Toll-like receptor 4-mediated activation of HIV long terminal repeat

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Monocytes/macrophages are known to represent a potential reservoir of human immunodeficiency virus type 1 (HIV-1), which ensures continuous replication of the virus in patients on highly active antiretroviral therapy (HAART). Infected macrophages are a highly productive source of HIV-1 during infections with common opportunistic pathogens. Previous studies report that toll like receptors (TLR)s play a role in HIV-1 replication in macrophages. Here, we investigate the three main pathways activated through TLR4 and the interactions with the HIV-1 long terminal repeat (LTR), using human embryonic kidney (HEK) 293 cells expressing TLR4 and transfected with a luciferase reporter under the control of the HIV-1 LTR. Here, we demonstrate, that TLR4-mediated activation of HIV-LTR is largely governed by the nuclear factor-κB pathway. Neither of the mitogen-activated protein kinases ERK1/2, JNK, or p38 nor the transcription factor interferon regulatory factor 3 were involved in the direct transactivation of HIV-LTR through stimulation of TLR4.

Original languageEnglish
Book seriesAPMIS
Pages (from-to)124-132
Number of pages9
Publication statusPublished - Feb 2009

    Research areas

  • Human immunodeficiency virus, Nuclear factor κB, Toll-like receptors

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