scholarly journals Toll-Like Receptor Agonists: Can They Exact a Toll on Human Immunodeficiency Virus Persistence?

2017 ◽  
Vol 64 (12) ◽  
pp. 1696-1698 ◽  
Author(s):  
Joshua C. Cyktor ◽  
John W. Mellors
Keyword(s):  
Human Immunodeficiency Virus ◽  
Toll Like Receptor ◽  
Virus Persistence ◽  
Receptor Agonists ◽  
Immunodeficiency Virus

scholarly journals Toll-Like Receptor 2 Promoter -196 to -174 Deletion Affects CD4 Levels Along Human Immunodeficiency Virus Infection Progression

2020 ◽  
Vol 222 (12) ◽  
pp. 2007-2011 ◽  
Author(s):  
Marina Laplana ◽  
Maria Jose Bravo ◽  
Marta Fernández-Fuertes ◽  
Celia Ruiz-Garcia ◽  
Emilio Alarcón-Martin ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Disease Progression ◽  
Cox Regression ◽  
Toll Like Receptor ◽  
Cox Regression Analysis ◽  
Immunodeficiency Virus ◽  
Toll Like Receptor 2 ◽  
Time Required ◽  
Molecular Patterns ◽  
Hiv 1

Abstract Toll-like receptor 2 (TLR2) plays a key role in innate immune response recognizing molecular patterns expressed by pathogens. rs111200466 is a TLR2 promoter insertion/deletion polymorphism with contradictory data about its role in human immunodeficiency virus type 1 (HIV-1) infection. We analyzed rs111200466 in HIV-1 disease progression and showed a correlation with a faster progression to the CD4+ < 200 cells/μL outcome for deletion allele carriers (Cox regression analysis: hazard ratio, 2.4 [95% confidence interval, 1.4–4]; P = .001). When naive patients with CD4+ < 200 cells/μL started antiretroviral treatment, rs111200466-deletion carriers showed a trend toward a slower, recovery rate (time required to reach CD4+ > 350 cells/μL; Cox P = .36). Our data suggest rs111200466 as a prognosis factor for HIV-1 disease progression.

Toll-like receptor pathway gene expression is associated with human immunodeficiency virus–associated neurodegeneration

2007 ◽  
Vol 13 (6) ◽  
pp. 496-503 ◽  
Author(s):  
Shahid Salaria ◽  
Haleh Badkoobehi ◽  
Edward Rockenstein ◽  
Leslie Crews ◽  
Gursharan Chana ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Immunodeficiency Virus ◽  
Toll Like Receptor ◽  
Pathway Gene ◽  
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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