scholarly journals 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 ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1299-1307 ◽  
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.

scholarly journals Penicillium marneffei-Stimulated Dendritic Cells Enhance HIV-1 Trans-Infection and Promote Viral Infection by Activating Primary CD4+ T Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e27609 ◽  
Author(s):  
Yan Qin ◽  
Yuye Li ◽  
Wan Liu ◽  
Renrong Tian ◽  
Qianqian Guo ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Viral Infection ◽  
Cd4 T Cells ◽  
Penicillium Marneffei ◽  
Trans Infection ◽  
Hiv 1

scholarly journals Myeloid and plasmacytoid dendritic cells transfer HIV-1 preferentially to antigen-specific CD4+ T cells

2005 ◽  
Vol 201 (12) ◽  
pp. 2023-2033 ◽  
Author(s):  
Karin Loré ◽  
Anna Smed-Sörensen ◽  
Jayanand Vasudevan ◽  
John R. Mascola ◽  
Richard A. Koup
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Immune Defense ◽  
Productive Infection ◽  
Specific Memory ◽  
Cell Immunity ◽  
Hiv 1

Dendritic cells (DCs) are essential antigen-presenting cells for the induction of T cell immunity against pathogens such as human immunodeficiency virus (HIV)-1. At the same time, HIV-1 replication is strongly enhanced in DC–T cell clusters, potentially undermining this process. We found that immature CD123+ plasmacytoid DCs (PDCs) and CD11c+ myeloid DCs (MDCs) were susceptible to both a CCR5- and a CXCR4-using HIV-1 isolate in vitro and were able to efficiently transfer that infection to autologous CD4+ T cells. Soon after HIV-1 exposure, both PDCs and MDCs were able to transfer the virus to T cells in the absence of a productive infection. However, once a productive infection was established in the DCs, newly synthesized virus was predominantly spread to T cells. HIV-1 exposure of the MDCs and PDCs did not inhibit their ability to present cytomegalovirus (CMV) antigens and activate CMV-specific memory T cells. As a result, both PDCs and MDCs preferentially transmitted HIV-1 to the responding CMV antigen–specific CD4+ T cells rather than to nonresponding T cells. This suggests that the induction of antigen-specific T cell responses by DCs, a process crucial to immune defense, can lead to preferential HIV-1 infection and the deletion of responding CD4+ T cells.

scholarly journals DC-SIGN–mediated Infectious Synapse Formation Enhances X4 HIV-1 Transmission from Dendritic Cells to T Cells

2004 ◽  
Vol 200 (10) ◽  
pp. 1279-1288 ◽  
Author(s):  
Jean-François Arrighi ◽  
Marjorie Pion ◽  
Eduardo Garcia ◽  
Jean-Michel Escola ◽  
Yvette van Kooyk ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Synapse Formation ◽  
Model Systems ◽  
Hiv 1 ◽  
Infectious Synapse

Dendritic cells (DCs) are essential for the early events of human immunodeficiency virus (HIV) infection. Model systems of HIV sexual transmission have shown that DCs expressing the DC-specific C-type lectin DC-SIGN capture and internalize HIV at mucosal surfaces and efficiently transfer HIV to CD4+ T cells in lymph nodes, where viral replication occurs. Upon DC–T cell clustering, internalized HIV accumulates on the DC side at the contact zone (infectious synapse), between DCs and T cells, whereas HIV receptors and coreceptors are enriched on the T cell side. Viral concentration at the infectious synapse may explain, at least in part, why DC transmission of HIV to T cells is so efficient. Here, we have investigated the role of DC-SIGN on primary DCs in X4 HIV-1 capture and transmission using small interfering RNA–expressing lentiviral vectors to specifically knockdown DC-SIGN. We demonstrate that DC-SIGN− DCs internalize X4 HIV-1 as well as DC-SIGN+ DCs, although binding of virions is reduced. Strikingly, DC-SIGN knockdown in DCs selectively impairs infectious synapse formation between DCs and resting CD4+ T cells, but does not prevent the formation of DC–T cells conjugates. Our results demonstrate that DC-SIGN is required downstream from viral capture for the formation of the infectious synapse between DCs and T cells. These findings provide a novel explanation for the role of DC-SIGN in the transfer and enhancement of HIV infection from DCs to T cells, a crucial step for HIV transmission and pathogenesis.

scholarly journals Unstimulated Primary CD4+ T Cells from HIV-1-Positive Elite Suppressors Are Fully Susceptible to HIV-1 Entry and Productive Infection

2010 ◽  
Vol 85 (2) ◽  
pp. 979-986 ◽  
Author(s):  
S. A. Rabi ◽  
K. A. O'Connell ◽  
D. Nikolaeva ◽  
J. R. Bailey ◽  
B. L. Jilek ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Productive Infection ◽  
Elite Suppressors ◽  
Hiv 1

scholarly journals Trans-infection but Not Infection from within Endosomal Compartments after Cell-to-cell HIV-1 Transfer to CD4+T Cells

2012 ◽  
Vol 287 (38) ◽  
pp. 32017-32026 ◽  
Author(s):  
Marc Permanyer ◽  
Ester Ballana ◽  
Roger Badia ◽  
Eduardo Pauls ◽  
Bonaventura Clotet ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Trans Infection ◽  
Hiv 1

scholarly journals Productive Infection of Plasmacytoid Dendritic Cells with Human Immunodeficiency Virus Type 1 Is Triggered by CD40 Ligation

2002 ◽  
Vol 76 (21) ◽  
pp. 11033-11041 ◽  
Author(s):  
Lawrence Fong ◽  
Manuela Mengozzi ◽  
Nancy W. Abbey ◽  
Brian G. Herndier ◽  
Edgar G. Engleman
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
Viral Replication ◽  
Cd4 T Cells ◽  
Cd40 Ligand ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Immature plasmacytoid dendritic cells are the principal alpha interferon-producing cells (IPC), responsible for primary antiviral immunity. IPC express surface molecules CD4, CCR5, and CXCR4, which are known coreceptors required for human immunodeficiency virus (HIV) infection. Here we show that IPC are susceptible to and replicate HIV type 1 (HIV-1). Importantly, viral replication is triggered upon activation of IPC with CD40 ligand, a signal physiologically delivered by CD4 T cells. Immunohistochemical staining of tonsil from HIV-infected individuals reveals HIV p24+ IPC, consistent with in vivo infection of these cells. IPC exposed in vitro to HIV produce alpha interferon, which partially inhibits viral replication. Nevertheless, IPC efficiently transmit HIV-1 to CD4 T-cells, and such transmission is also augmented by CD40 ligand activation. IPC produce RANTES/CCL5 and MIP-1α/CCL3 when exposed to HIV in vitro. IPC also induce naïve CD4 T cells to proliferate and would therefore preferentially infect these cells. These results indicate that IPC may play an important role in the dissemination of HIV.

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