Human immunodeficiency virus type 1 Tat induces B7-H1 expression via ERK/MAPK signaling pathway

2011 ◽  
Vol 271 (2) ◽  
pp. 280-285 ◽  
Author(s):  
Jijing Shi ◽  
Xiaolin Qin ◽  
Lin Zhao ◽  
Gongze Wang ◽  
Chaoqi Liu
Keyword(s):  
Human Immunodeficiency Virus ◽  
Signaling Pathway ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Erk Mapk ◽  
Immunodeficiency Virus

scholarly journals Binding of Human Immunodeficiency Virus Type 1 to CD4 and CXCR4 Receptors Differentially Regulates Expression of Inflammatory Genes and Activates the MEK/ERK Signaling Pathway

1998 ◽  
Vol 72 (8) ◽  
pp. 6406-6413 ◽  
Author(s):  
Waldemar Popik ◽  
Joseph E. Hesselgesser ◽  
Paula M. Pitha
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Signaling Pathway ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immunodeficiency Virus ◽  
Map Kinase Pathway ◽  
Kinase Pathway ◽  
Hiv 1

ABSTRACT We have previously shown that binding of human immunodeficiency virus type 1 (HIV-1) virions to CD4 receptors stimulates association of Lck with Raf-1 and results in the activation of Raf-1 kinase in a Ras-independent manner. In the present study, we demonstrate that HIV-1 envelope glycoproteins of both T-cell-tropic and macrophagetropic strains rapidly activate the ERK/mitogen-activated protein (MAP) kinase pathway and the binding of nuclear transcription factors (AP-1, NF-κB, and C/EBP) and stimulate expression of cytokine and chemokine genes. The activation of this signaling pathway requires functional CD4 receptors and is independent of binding to CXCR4. Binding of the natural ligand stromal cell-derived factor 1 (SDF-1) to CXCR4, which inhibits entry of T-cell-tropic HIV-1, activates also the ERK/MAP kinase pathway. However, SDF-1 did not affect the CD4-mediated expression of cytokine and chemokine genes. These results provide firm molecular evidence that binding of HIV-1 envelope glycoproteins to CD4 receptor initiates a signaling pathway(s) independent of the binding to the chemokine receptor that leads to the aberrant expression of inflammatory genes and may contribute significantly to HIV-1 replication as well as to deregulation of the immune system.

scholarly journals Single-Cell, Phosphoepitope-Specific Analysis Demonstrates Cell Type- and Pathway-Specific Dysregulation of Jak/STAT and MAPK Signaling Associated with In Vivo Human Immunodeficiency Virus Type 1 Infection

2008 ◽  
Vol 82 (7) ◽  
pp. 3702-3712 ◽  
Author(s):  
Andrew W. Lee ◽  
Elizabeth R. Sharp ◽  
Alison O'Mahony ◽  
Michael G. Rosenberg ◽  
Dennis M. Israelski ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Single Cell ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Mapk Signaling ◽  
Cell Type ◽  
Gm Csf ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Despite extensive evidence of cell signaling alterations induced by human immunodeficiency virus type 1 (HIV-1) in vitro, the relevance of these changes to the clinical and/or immunologic status of HIV-1-infected individuals is often unclear. As such, mapping the details of cell type-specific degradation of immune function as a consequence of changes to signaling network responses has not been readily accessible. We used a flow cytometric-based assay of signaling to determine Janus kinase/signal transducers and activators of transcription (Jak/STAT) signaling changes at the single-cell level within distinct cell subsets from the primary immune cells of HIV-1-infected donors. We identified a specific defect in granulocyte-macrophage colony-stimulating factor (GM-CSF)-driven Stat5 phosphorylation in the monocytes of HIV-1+ donors. This inhibition was statistically significant in a cohort of treated and untreated individuals. Ex vivo Stat5 phosphorylation levels varied among HIV-1+ donors but did not correlate with CD4+ T-cell counts or HIV-1 plasma viral load. Low Stat5 activation occurred in HIV-1-infected donors despite normal GM-CSF receptor levels. Investigation of mitogen-activated protein kinase (MAPK) pathways, also stimulated by GM-CSF, led to the observation that lipopolysaccharide-stimulated extracellular signal-regulated kinase phosphorylation is enhanced in monocytes. Thus, we have identified a specific, imbalanced monocyte signaling profile, with inhibition of STAT and enhancement of MAPK signaling, associated with HIV-1 infection. This understanding of altered monocyte signaling responses that contribute to defective antigen presentation during HIV-1 infection could lead to immunotherapeutic approaches that compensate for the deficiency.

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