scholarly journals Toll-Like Receptor 8 Ligands Activate a Vitamin D Mediated Autophagic Response that Inhibits Human Immunodeficiency Virus Type 1

2012 ◽  
Vol 8 (11) ◽  
pp. e1003017 ◽  
Author(s):  
Grant R. Campbell ◽  
Stephen A. Spector
Keyword(s):  
Vitamin D ◽  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Toll Like Receptor ◽  
Immunodeficiency Virus

scholarly journals MyD88-Dependent Immune Activation Mediated by Human Immunodeficiency Virus Type 1-Encoded Toll-Like Receptor Ligands

2007 ◽  
Vol 81 (15) ◽  
pp. 8180-8191 ◽  
Author(s):  
Angela Meier ◽  
Galit Alter ◽  
Nicole Frahm ◽  
Harlyn Sidhu ◽  
Bin Li ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
T Cell Activation ◽  
Immune Activation ◽  
Plasmacytoid Dendritic Cell ◽  
Toll Like Receptor ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Immune activation is a major characteristic of human immunodeficiency virus type 1 (HIV-1) infection and a strong prognostic factor for HIV-1 disease progression. The underlying mechanisms leading to immune activation in viremic HIV-1 infection, however, are not fully understood. Here we show that, following the initiation of highly active antiretroviral therapy, the immediate decline of immune activation is closely associated with the reduction of HIV-1 viremia, which suggests a direct contribution of HIV-1 itself to immune activation. To propose a mechanism, we demonstrate that the single-stranded RNA of HIV-1 encodes multiple uridine-rich Toll-like receptor 7/8 (TLR7/8) ligands that induce strong MyD88-dependent plasmacytoid dendritic cell and monocyte activation, as well as accessory cell-dependent T-cell activation. HIV-1-encoded TLR ligands may, therefore, directly contribute to the immune activation observed during viremic HIV-1 infection. These data provide an initial rationale for inhibiting the TLR pathway to directly reduce the chronic immune activation induced by HIV-1 and the associated immune pathogenesis.

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