Effect of mucosal fluid from women with bacterial vaginosis on HIV trans-infection mediated by dendritic cells

Bacterial vaginosis (BV), the most common genital infection in reproductive-aged women, is associated with increased risk of sexually transmitted infections. Its etiology remains unclear, especially the role ofGardnerella(G.)vaginalis, an anaerobic bacterium characteristic of the BV-alteration of the vaginal ecosystem. In the genital mucosa, dendritic cells (DCs) sense bacteria of the microenvironmentviareceptors and then orchestrate the immune response by induction of different T cell subtypes. We investigated the interactions betweenG. vaginalisand human monocyte-derived DCs using a wide range of bacterial concentrations (multiplicity of infection from 0.01 to 100), and the effects of this pathogen on PHA-induced lymphocyte proliferation. As observed by electron microscopy and cytometry,G. vaginalisreduced the internalization ability of DCs by forming extracellular clusters and induced neither DC maturation, nor DC secretion of cytokines, except at the highest dose with a very early DC maturation state. The same profile was observed on lymphocytes with significant increases of proliferation and cytokine secretion only at the highest bacterial concentration. Our findings indicate thatG. vaginalispossesses slight immune-stimulating activities against DCs and T cells, reflecting thus a defective inflammatory response and giving rise to the atypical, non- or low-grade, inflammatory clinical disease profile.

Download Full-text

The C-type lectin surface receptor DCIR acts as a new attachment factor for HIV-1 in dendritic cells and contributes to trans- and cis-infection pathways

Blood ◽

10.1182/blood-2008-01-136473 ◽

2008 ◽

Vol 112 (4) ◽

pp. 1299-1307 ◽

Cited By ~ 125

Author(s):

Alexandra A. Lambert ◽

Caroline Gilbert ◽

Manon Richard ◽

André D. Beaulieu ◽

Michel J. Tremblay

Keyword(s):

T Cells ◽

Dendritic Cells ◽

Cd4 T Cells ◽

Productive Infection ◽

Virus Binding ◽

Virus Propagation ◽

Cell Surface Molecule ◽

Lectin Receptor ◽

Trans Infection ◽

Hiv 1

Abstract The dynamic interplay between dendritic cells (DCs) and human immunodeficiency virus type-1 (HIV-1) is thought to result in viral dissemination and evasion of antiviral immunity. Although initial observations suggested that the C-type lectin receptor (CLR) DC-SIGN was responsible for the trans-infection function of the virus, subsequent studies demonstrated that trans-infection of CD4+ T cells with HIV-1 can also occur through DC-SIGN–independent mechanisms. We demonstrate that a cell surface molecule designated DCIR (for DCimmunoreceptor), a member of a recently described family of DC-expressing CLRs, can participate in the capture of HIV-1 and promote infection in trans and in cis of autologous CD4+ T cells from human immature monocyte-derived DCs. The contribution of DCIR to these processes was revealed using DCIR-specific siRNAs and a polyclonal antibody specific for the carbohydrate recognition domain of DCIR. Data from transfection experiments indicated that DCIR acts as a ligand for HIV-1 and is involved in events leading to productive virus infection. Finally, we show that the neck domain of DCIR is important for the DCIR-mediated effect on virus binding and infection. These results point to a possible role for DCIR in HIV-1 pathogenesis by supporting the productive infection of DCs and promoting virus propagation.

Download Full-text

Kaposi's-sarcoma-associated-herpesvirus-activated dendritic cells promote HIV-1 trans-infection and suppress CD4+ T cell proliferation

Virology ◽

10.1016/j.virol.2013.02.018 ◽

2013 ◽

Vol 440 (2) ◽

pp. 150-159 ◽

Cited By ~ 1

Author(s):

Wan Liu ◽

Yan Qin ◽

Lei Bai ◽

Ke Lan ◽

Jian-Hua Wang

Keyword(s):

Cell Proliferation ◽

Dendritic Cells ◽

T Cell ◽

Kaposi's Sarcoma ◽

Kaposi’S Sarcoma ◽

Cd4 T Cell ◽

T Cell Proliferation ◽

Trans Infection ◽

Kaposi’S Sarcoma Associated Herpesvirus ◽

Hiv 1

Download Full-text

922 HIV-1 trans-infection of T-cells via dendritic cells requires endosomal sorting and polarized trafficking to the virological synapse

Journal of Investigative Dermatology ◽

10.1016/j.jid.2018.03.934 ◽

2018 ◽

Vol 138 (5) ◽

pp. S157

Author(s):

R. Bayliss ◽

J. Wheeldon ◽

S. Caucheteux ◽

C. Niessen ◽

V. Piguet

Keyword(s):

T Cells ◽

Dendritic Cells ◽

Virological Synapse ◽

Endosomal Sorting ◽

Trans Infection ◽

Polarized Trafficking ◽

Hiv 1

Download Full-text

Uterine Epithelial Cell Regulation of DC-SIGN Expression Inhibits Transmitted/Founder HIV-1 Trans Infection by Immature Dendritic Cells

PLoS ONE ◽

10.1371/journal.pone.0014306 ◽

2010 ◽

Vol 5 (12) ◽

pp. e14306 ◽

Cited By ~ 25

Author(s):

Daniel O. Ochiel ◽

Christina Ochsenbauer ◽

John C. Kappes ◽

Mimi Ghosh ◽

John V. Fahey ◽

...

Keyword(s):

Dendritic Cells ◽

Epithelial Cell ◽

Cell Regulation ◽

Uterine Epithelial Cell ◽

Immature Dendritic Cells ◽

Trans Infection ◽

Hiv 1

Download Full-text

Capture and transfer of HIV-1 particles by mature dendritic cells converges with the exosome-dissemination pathway

Blood ◽

10.1182/blood-2008-05-158642 ◽

2009 ◽

Vol 113 (12) ◽

pp. 2732-2741 ◽

Cited By ~ 148

Author(s):

Nuria Izquierdo-Useros ◽

Mar Naranjo-Gómez ◽

Jacob Archer ◽

Steven C. Hatch ◽

Itziar Erkizia ◽

...

Keyword(s):

Dendritic Cells ◽

T Lymphocytes ◽

T Cell Activation ◽

Cell Activation ◽

Fluorescent Protein ◽

Independent Manner ◽

Trans Infection ◽

Immunodeficiency Virus ◽

Green Fluorescent ◽

Hiv 1

AbstractExosomes are secreted cellular vesicles that can be internalized by dendritic cells (DCs), contributing to antigen-specific naive CD4+ T-cell activation. Here, we demonstrate that human immunodeficiency virus type 1 (HIV-1) can exploit this exosome antigen-dissemination pathway intrinsic to mature DCs (mDCs) for mediating trans-infection of T lymphocytes. Capture of HIV-1, HIV-1 Gag-enhanced green fluorescent protein (eGFP) viral-like particles (VLPs), and exosomes by DCs was up-regulated upon maturation, resulting in localization within a CD81+ compartment. Uptake of VLPs or exosomes could be inhibited by a challenge with either particle, suggesting that the expression of common determinant(s) on VLP or exosome surface is necessary for internalization by mDCs. Capture by mDCs was insensitive to proteolysis but blocked when virus, VLPs, or exosomes were produced from cells treated with sphingolipid biosynthesis inhibitors that modulate the lipid composition of the budding particles. Finally, VLPs and exosomes captured by mDCs were transmitted to T lymphocytes in an envelope glycoprotein-independent manner, underscoring a new potential viral dissemination pathway.

Download Full-text