Faculty Opinions recommendation of MyD88-dependent immune activation mediated by human immunodeficiency virus type 1-encoded Toll-like receptor ligands.

2007 ◽  
Author(s):  
Alan Landay
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immune Activation ◽  
Toll Like Receptor ◽  
Receptor Ligands ◽  
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.

scholarly journals Lymphatic Tissue Fibrosis Is Associated with Reduced Numbers of Naïve CD4+ T Cells in Human Immunodeficiency Virus Type 1 Infection

2006 ◽  
Vol 13 (5) ◽  
pp. 556-560 ◽  
Author(s):  
Timothy W. Schacker ◽  
Jason M. Brenchley ◽  
Gregory J. Beilman ◽  
Cavan Reilly ◽  
Stefan E. Pambuccian ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immune Activation ◽  
Cellular Interactions ◽  
Collagen Deposition ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The organized structure of lymphatic tissues (LTs) constitutes a microenvironment referred to as a niche that plays a critical role in immune system homeostasis by promoting cellular interactions and providing access to cytokines and growth factors on which cells are dependent for survival, proliferation, and differentiation. In chronic human immunodeficiency virus type 1 (HIV-1) infection, immune activation and inflammation result in collagen deposition and disruption of this LT niche. We have previously shown that these fibrotic changes correlate with a reduction in the size of the total population of CD4+ T cells. We now show that this reduction is most substantial within the naïve CD4+ T-cell population and is in proportion to the extent of LT collagen deposition in HIV-1 infection. Thus, the previously documented depletion of naïve CD4+ T cells in LTs in HIV-1 infection may be a consequence not only of a decreased supply of thymic emigrants or chronic immune activation but also of the decreased ability of those cells to survive in a scarred LT niche. We speculate that LT collagen deposition might therefore limit repopulation of naïve CD4+ T cells with highly active antiretroviral therapy, and thus, additional treatments directed to limiting or reversing inflammatory damage to the LT niche could potentially improve immune reconstitution.

scholarly journals Correlation between Human Immunodeficiency Virus Type 1 RNA Levels in the Female Genital Tract and Immune Activation Associated with Ulceration of the Cervix

2000 ◽  
Vol 181 (6) ◽  
pp. 1950-1956 ◽  
Author(s):  
Stephen D. Lawn ◽  
Shambavi Subbarao ◽  
Thomas C. Wright, Jr. ◽  
Tammy Evans‐Strickfaden ◽  
Tedd V. Ellerbrock ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immune Activation ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Immunodeficiency Virus ◽  
Female Genital ◽  
Rna Levels
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