Follicular dendritic cells and human immunodeficiency virus infectivity

Nature ◽  
1995 ◽  
Vol 377 (6551) ◽  
pp. 740-744 ◽  
Author(s):  
Sonya L. Heath ◽  
J. Grant Tew ◽  
John G. Tew ◽  
Andras K. Szakal ◽  
Gregory F. Burton
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dendritic Cells ◽  
Virus Infectivity ◽  
Follicular Dendritic Cells ◽  
Immunodeficiency Virus ◽  
Follicular Dendritic

scholarly journals Follicular Dendritic Cells and Human Immunodeficiency Virus Type 1 Transcription in CD4+ T Cells

2008 ◽  
Vol 83 (1) ◽  
pp. 150-158 ◽  
Author(s):  
Tyler C. Thacker ◽  
Xueyuan Zhou ◽  
Jacob D. Estes ◽  
Yongjun Jiang ◽  
Brandon F. Keele ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
Ex Vivo ◽  
Follicular Dendritic Cells ◽  
Hiv Replication ◽  
Hiv Transcription ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Follicular Dendritic

ABSTRACT HIV replication occurs throughout the natural course of infection in secondary lymphoid tissues and in particular within the germinal centers (GCs), where follicular dendritic cells (FDCs) are adjacent to CD4+ T cells. Because FDCs provide signaling that increases lymphocyte activation, we postulated that FDCs could increase human immunodeficiency virus (HIV) replication. We cultured HIV-infected CD4+ T cells alone or with FDCs and measured subsequent virus expression using HIV-p24 production and reverse transcription-PCR analyses. When cultured with FDCs, infected CD4+ T cells produced almost fourfold more HIV than when cultured alone, and the rate of virus transcription was doubled. Both FDCs and their supernatant increased HIV transcription and resulted in nuclear translocation of NF-κB and phosphorylated c-Jun in infected cells. FDCs produced soluble tumor necrosis factor alpha (TNF-α) ex vivo, and the addition of a blocking soluble TNF receptor ablated FDC-mediated HIV transcription. Furthermore, TNF-α was found highly expressed within GCs, and ex vivo GC CD4+ T cells supported greater levels of HIV-1 replication than other CD4+ T cells. These data indicated that FDCs increase HIV transcription and production by a soluble TNF-α-mediated mechanism. This FDC-mediated effect may account, at least in part, for the presence of persistent HIV replication in GCs. Therefore, in addition to providing an important reservoir of infectious virus, FDCs increase HIV production, contributing to a tissue microenvironment that is highly conducive to HIV transmission and expression.

Isolation of normal human follicular dendritic cells and CD4-independentin vitro infection by human immunodeficiency virus (HIV-1)

1991 ◽  
Vol 21 (8) ◽  
pp. 1873-1878 ◽  
Author(s):  
Ingrid Stahmer ◽  
J. Pascal Zimmer ◽  
Martin Ernst ◽  
Thomas Fenner ◽  
Ricarda Finnern ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dendritic Cells ◽  
Follicular Dendritic Cells ◽  
Immunodeficiency Virus ◽  
Normal Human ◽  
Follicular Dendritic ◽  
Hiv 1

scholarly journals Human Follicular Dendritic Cells Remain Uninfected and Capture Human Immunodeficiency Virus Type 1 through CD54-CD11a Interaction

1999 ◽  
Vol 73 (5) ◽  
pp. 3603-3607 ◽  
Author(s):  
Masatoshi Fujiwara ◽  
Rikiya Tsunoda ◽  
Shiro Shigeta ◽  
Tomoyuki Yokota ◽  
Masanori Baba
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Follicular Dendritic Cells ◽  
Immunodeficiency Virus ◽  
Follicular Dendritic ◽  
Hiv 1

ABSTRACT It has been reported that human immunodeficiency virus type 1 (HIV-1) bound to follicular dendritic cells (FDCs) remains highly infectious to CD4+ T cells even when it forms immune complexes with neutralizing antibody (HIV-1/IC). To elucidate the role of FDCs in HIV-1 transmission to CD4+ T cells in lymph nodes, we have isolated and purified FDCs from human tonsils and examined whether the HIV-1/IC trapped on their surface is infectious to CD4+ T cells. To our surprise, not the HIV-1/IC but the antibody-free HIV-1 on FDCs could be transmitted to CD4+ T cells. Furthermore, in contrast to previous studies showing that FDCs are productively infected with HIV-1, the present study clearly demonstrated that FDCs were not the target cells for HIV-1 infection. FDCs could capture the viral particles on their surface; however, the binding of HIV-1 to FDCs was strongly inhibited by the presence of anti-CD54 (ICAM-1) monoclonal antibody (MAb) and anti-CD11a (LFA-1) MAb, suggesting that the adhesion molecules play an important role in the interaction between HIV-1 and FDCs.

scholarly journals Influence of follicular dendritic cells on HIV dynamics

2000 ◽  
Vol 355 (1400) ◽  
pp. 1051-1058 ◽  
Author(s):  
William S. Hlavacek ◽  
Nikolaos I. Stilianakis ◽  
Alan S. Perelson
Keyword(s):  
Dendritic Cells ◽  
Reverse Transcriptase ◽  
Lymphoid Tissue ◽  
Follicular Dendritic Cells ◽  
Plasma Virus ◽  
Immunodeficiency Virus ◽  
Infected Cells ◽  
Follicular Dendritic ◽  
Hiv 1

In patients infected with human immunodeficiency virus type 1 (HIV-1), a large amount of virus is associated with follicular dendritic cells (FDCs) in lymphoid tissue. To assess the influence of FDCs on viral dynamics during antiretroviral therapy, we have developed a mathematical model for treatment of HIV-1 infection that includes FDCs. Here, we use this model to analyse measurements of HIV-1 dynamics in the blood and lymphoid tissue of a representative patient, who was treated with a combination of HIV-1 reverse transcriptase and protease inhibitors. We show that loss of virus from FDCs during therapy can make a much larger contribution to plasma virus than production of virus by infected cells. This result challenges the notion that long-lived infected cells are a significant source of HIV-1 during drug therapy. Due to release of FDC-associated virus, we find that it is necessary to revise upward previous estimates of c , the rate at which free virus is cleared, and δ , the rate at which productively infected cells die. Furthermore, we find that potentially infectious virus, present before treatment, is released from FDCs during therapy and that the persistence of this virus can be affected by whether therapy includes reverse transcriptase inhibitors.

Sign in / Sign up

Export Citation Format

Share Document