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

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Abstract:

Berg RS, Aggerholm A, Bertelsen LS, Østergaard L, Paludan SR. Role of mitogen-activated protein kinases, nuclear factor-B, and interferon regulatory factor 3 in Toll-like receptor 4-mediated activation of HIV long terminal repeat. APMIS 2009; 117: 124–32.

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-B 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.

Keywords: Toll-like receptors; human immunodeficiency virus; nuclear factor B

Document Type: Research Article

DOI: https://doi.org/10.1111/j.1600-0463.2008.00024.x

Affiliations: 1: Department of Infectious Diseases, Skejby Hospital, Aarhus; and 2: Institute of Medical Microbiology and Immunology, University of Aarhus, Denmark

Publication date: 2009-02-01

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