scholarly journals Dendritic Cells in HIV-1 and HCV Infection: Can They Help Win the Battle?

2013 ◽  
Vol 4 ◽  
pp. VRT.S11046 ◽  
Author(s):  
Mohit Sehgal ◽  
Zafar K. Khan ◽  
Andrew H. Talal ◽  
Pooja Jain
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Immunological Synapse ◽  
Hcv Infection ◽  
Dc Functions ◽  
Antiviral Immune Response ◽  
Persistent Infections ◽  
Viral Therapy ◽  
Host Genetic ◽  
Hiv 1

Persistent infections with human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) are a major cause of morbidity and mortality worldwide. As sentinels of our immune system, dendritic cells (DCs) play a central role in initiating and regulating a potent antiviral immune response. Recent advances in our understanding of the role of DCs during HIV-1 and HCV infection have provided crucial insights into the mechanisms employed by these viruses to impair DC functions in order to evade an effective immune response against them. Modulation of the immunological synapse between DC and T-cell, as well as dysregulation of the crosstalk between DCs and natural killer (NK) cells, are emerging as two crucial mechanisms. This review focuses on understanding the interaction of HIV-1 and HCV with DCs not only to understand the immunopathogenesis of chronic HIV-1 and HCV infection, but also to explore the possibilities of DC-based immunotherapeutic approaches against them. Host genetic makeup is known to play major roles in infection outcome and rate of disease progression, as well as response to anti-viral therapy in both HIV-1 and HCV-infected individuals. Therefore, we highlight the genetic variations that can potentially affect DC functions, especially in the setting of chronic viral infection. Altogether, we address if DCs’ potential as critical effectors of antiviral immune response could indeed be utilized to combat chronic infection with HIV-1 and HCV.

scholarly journals Dendritic Cell Precursors Are Permissive to Dengue Virus and Human Immunodeficiency Virus Infection

2005 ◽  
Vol 79 (12) ◽  
pp. 7291-7299 ◽  
Author(s):  
Wing-Hong Kwan ◽  
Anna-Marija Helt ◽  
Concepción Marañón ◽  
Jean-Baptiste Barbaroux ◽  
Anne Hosmalin ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Dengue Virus ◽  
Blood Monocytes ◽  
Dengue Virus Infection ◽  
Differentiation Potential ◽  
Antiviral Immune Response ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT CD14+ interstitial cells reside beneath the epidermis of skin and mucosal tissue and may therefore play an important role in viral infections and the shaping of an antiviral immune response. However, in contrast to dendritic cells (DC) or blood monocytes, these antigen-presenting cells (APC) have not been well studied. We have previously described long-lived CD14+ cells generated from CD34+ hematopoietic progenitors, which may represent model cells for interstitial CD14+ APC. Here, we show that these cells carry DC-SIGN and differentiate into immature DC in the presence of granulocyte-macrophage colony-stimulating factor. We have compared the CD14+ cells and the DC derived from these cells with respect to dengue virus and human immunodeficiency virus type 1 (HIV-1) infection. Both cell types are permissive to dengue virus infection, but the CD14+ cells secrete the anti-inflammatory cytokine interleukin 10 and no tumor necrosis factor alpha. Regarding HIV, the CD14+ cells are permissive to HIV-1, release higher p24 levels than the derived DC, and more efficiently activate HIV Pol-specific CD8+ memory T cells. The CD14+ DC precursors infected with either virus retain their DC differentiation potential. The results suggest that interstitial CD14+ APC may contribute to HIV-1 and dengue virus infection and the shaping of an antiviral immune response.

scholarly journals TLR Activation of Langerhans Cell-Like Dendritic Cells Triggers an Antiviral Immune Response

2006 ◽  
Vol 177 (1) ◽  
pp. 298-305 ◽  
Author(s):  
Claudia N. Renn ◽  
David Jesse Sanchez ◽  
Maria Teresa Ochoa ◽  
Annaliza J. Legaspi ◽  
Chang-Keun Oh ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Langerhans Cell ◽  
Antiviral Immune Response

scholarly journals HIV-1 Tat Addresses Dendritic Cells to Induce a Predominant Th1-Type Adaptive Immune Response That Appears Prevalent in the Asymptomatic Stage of Infection

2009 ◽  
Vol 182 (5) ◽  
pp. 2888-2897 ◽  
Author(s):  
Emanuele Fanales-Belasio ◽  
Sonia Moretti ◽  
Valeria Fiorelli ◽  
Antonella Tripiciano ◽  
Maria R. Pavone Cossut ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Asymptomatic Stage ◽  
Hiv 1

[457] HCV INFECTION OF DENDRITIC CELLS AFFECTS THEIR FUNCTION LEADING TO AN IMPAIRED ADAPTIVE IMMUNE RESPONSE

2007 ◽  
Vol 46 ◽  
pp. S174
Author(s):  
I. Pachiadakis ◽  
S. Choksi ◽  
H. Cooksley ◽  
C. Sarrazzin ◽  
S. Zeuzem ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Adaptive Immune Response ◽  
Hcv Infection ◽  
Adaptive Immune

Human dendritic cells promote an antiviral immune response when stimulated by CVT-E002

2011 ◽  
Vol 63 (5) ◽  
pp. 670-678 ◽  
Author(s):  
Ramses Ilarraza ◽  
Yingqi Wu ◽  
Francis Davoine ◽  
Cory Ebeling ◽  
Darryl J. Adamko
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Antiviral Immune Response ◽  
Human Dendritic Cells

scholarly journals Plasmacytoid dendritic cells and their role in the immunopathogenesis of viral infections for example hepatitis B

2019 ◽  
Vol 11 (2) ◽  
pp. 14-19 ◽  
Author(s):  
R. R. Khodzhibekov ◽  
O. N. Khokhlova ◽  
A. R. Reizis ◽  
G. M. Kozhevnikova
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Unique Type ◽  
Antiviral Immune Response ◽  
Chronic Hbv Infection ◽  
B Virus ◽  
Chronic Hbv

A new approach in understanding the mechanisms of immune response in viral hepatitis is the discovery of a unique type of immune cells – plasmocytoid dendritic cells (pDCs). Plasmocytoid dendritic cells (pDCs) are cells of lymphoid origin and morphologically resemble plasma cells. Functionally, they are professional IFN-a-producing cells that play an important role in antiviral immune response. Data on the mechanisms of PDCs participation in hepatitis B virus infection are few and contradictory. In chronic HBV infection, the role of pDCs remains mysterious and poorly understood with conflicting circulating blood pDCs results that show differently that they are not affected or reduced. However, functional disorders of pDCs were observed in patients with chronic HBV infection. The establishment of these mechanisms, as well as the search for the cause of hepatitis B virus latency and the formation of chronic infection remains one of the important and promising areas of scientific activities today.

scholarly journals Antiviral and Immunoregulatory Effects of Indoleamine-2,3-Dioxygenase in Hepatitis C Virus Infection

2015 ◽  
Vol 7 (5) ◽  
pp. 530-544 ◽  
Author(s):  
Quentin Lepiller ◽  
Eric Soulier ◽  
Qisheng Li ◽  
Mélanie Lambotin ◽  
Jochen Barths ◽  
...  
Keyword(s):  
Immune Response ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Inhibitory Effect ◽  
Hcv Infection ◽  
Antiviral Immune Response ◽  
Host Immune Responses ◽  
Indoleamine 2,3 Dioxygenase ◽  
Important Regulator ◽  
Innate Defence

In patients with hepatitis C virus (HCV) infection, enhanced activity of indoleamine-2,3-dioxygenase 1 (IDO) has been reported. IDO - a tryptophan-catabolizing enzyme - has been considered as both an innate defence mechanism and an important regulator of the immune response. The molecular mechanism of IDO induction in HCV infection and its role in the antiviral immune response remain unknown. Using primary human hepatocytes, we show that HCV infection stimulates IDO expression. IDO gene induction was transient and coincided with the expression of types I and III interferons (IFNs) and IFN-stimulated genes in HCV-infected hepatocytes. Overexpression of hepatic IDO prior to HCV infection markedly impaired HCV replication in hepatocytes, suggesting that IDO limits the spread of HCV within the liver. siRNA-mediated IDO knock-down revealed that IDO functions as an IFN-mediated anti-HCV effector. Hepatic IDO was most potently induced by IFN-γ, and ongoing HCV replication could significantly upregulate IDO expression. IRF1 (IFN-regulatory factor 1) and STAT1 (signal transducer and activator of transcription 1) regulated hepatic IDO expression. Hepatic IDO expression also had a significant inhibitory effect on CD4+ T-cell proliferation. Our data suggest that hepatic IDO plays a dual role during HCV infection by slowing down viral replication and also regulating host immune responses.

scholarly journals Protease Cleavage Sites in HIV-1 gp120 Recognized by Antigen Processing Enzymes Are Conserved and Located at Receptor Binding Sites

2009 ◽  
Vol 84 (3) ◽  
pp. 1513-1526 ◽  
Author(s):  
Bin Yu ◽  
Dora P. A. J. Fonseca ◽  
Sara M. O'Rourke ◽  
Phillip W. Berman
Keyword(s):  
Immune Response ◽  
Receptor Binding ◽  
Neutralizing Antibodies ◽  
Antigen Processing ◽  
Cleavage Sites ◽  
Antiviral Immune Response ◽  
Processing Enzymes ◽  
Protease Cleavage ◽  
Protease Cleavage Sites ◽  
Hiv 1

ABSTRACT The identification of vaccine immunogens able to elicit broadly neutralizing antibodies (bNAbs) is a major goal in HIV vaccine research. Although it has been possible to produce recombinant envelope glycoproteins able to adsorb bNAbs from HIV-positive sera, immunization with these proteins has failed to elicit antibody responses effective against clinical isolates of HIV-1. Thus, the epitopes recognized by bNAbs are present on recombinant proteins, but they are not immunogenic. These results led us to consider the possibility that changes in the pattern of antigen processing might alter the immune response to the envelope glycoprotein to better elicit protective immunity. In these studies, we have defined protease cleavage sites on HIV gp120 recognized by three major human proteases (cathepsins L, S, and D) important for antigen processing and presentation. Remarkably, six of the eight sites identified in gp120 were highly conserved and clustered in regions of the molecule associated with receptor binding and/or the binding of neutralizing antibodies. These results suggested that HIV may have evolved to take advantage of major histocompatibility complex (MHC) class II antigen processing enzymes in order to evade or direct the antiviral immune response.

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