Progressive B Cell Apoptosis and Expression of Fas Ligand during Human Immunodeficiency Virus Type 1 Infection

1997 ◽  
Vol 13 (12) ◽  
pp. 1031-1038 ◽  
Author(s):  
ASTRID SAMUELSSON ◽  
ANDERS SÖNNERBORG ◽  
NICOLE HEUTS ◽  
JOAKIM CÖSTER ◽  
FRANCESCA CHIODI
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cell ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Cell Apoptosis ◽  
Fas Ligand ◽  
Immunodeficiency Virus

scholarly journals Human immunodeficiency virus type-1 induces a regulatory B cell-like phenotype in vitro

2017 ◽  
Vol 15 (10) ◽  
pp. 917-933 ◽  
Author(s):  
Jacobo Lopez-Abente ◽  
Adrián Prieto-Sanchez ◽  
Maria-Ángeles Muñoz-Fernandez ◽  
Rafael Correa-Rocha ◽  
Marjorie Pion
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cell ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Regulatory B Cell ◽  
Immunodeficiency Virus

scholarly journals Human Immunodeficiency Virus Type 1-Associated CD40 Ligand Transactivates B Lymphocytes and Promotes Infection of CD4+ T Cells

2007 ◽  
Vol 81 (11) ◽  
pp. 5872-5881 ◽  
Author(s):  
Geneviève Martin ◽  
Jocelyn Roy ◽  
Corinne Barat ◽  
Michel Ouellet ◽  
Caroline Gilbert ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cell ◽  
B Lymphocytes ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Nuclear Translocation ◽  
Cd40 Ligand ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Abnormal activation of B lymphocytes is a feature commonly seen in human immunodeficiency virus type 1 (HIV-1)-infected persons. However, the mechanism(s) responsible for this dysfunction is still poorly understood. Having recently shown that CD40L, the ligand for CD40, is inserted within emerging HIV-1 particles, we hypothesized that the contact between virus-anchored host CD40L and CD40 on the surface of B lymphocytes might result in the activation of this cell type. We report here that CD40L-bearing viruses, but not isogenic virions lacking host-derived CD40L, can induce immunoglobulin G and interleukin-6 production. Furthermore, such viral entities were found to induce B-cell homotypic adhesion. These effects were paralleled at the intracellular level by the nuclear translocation of the ubiquitous transcription factor NF-κB. The presence of host-derived CD40L within virions resulted in an increased virus attachment to B cells and a more-efficient B-cell-mediated transfer of HIV-1 to autologous CD4+ T lymphocytes. All the above processes were independent of the virus-encoded envelope glycoproteins. Altogether, the data gathered from this series of investigations suggest that the incorporation of host-encoded CD40L in HIV-1 is likely to play a role in the B-cell abnormalities that are seen in infected individuals.

Generation of a human immunodeficiency virus type 1 chronically infected monkey B cell line expressing low levels of endogenous TRIM5α

2009 ◽  
Vol 221 (3) ◽  
pp. 760-765 ◽  
Author(s):  
Barbara Ridolfi ◽  
Stefania Catone ◽  
Marco Sgarbanti ◽  
Leonardo Sernicola ◽  
Angela Battistini ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cell ◽  
Cell Line ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Infected Monkey ◽  
Immunodeficiency Virus ◽  
Low Levels

scholarly journals Shaping T Cell – B Cell Collaboration in the Response to Human Immunodeficiency Virus Type 1 Envelope Glycoprotein gp120 by Peptide Priming

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65748 ◽  
Author(s):  
N. Kalaya Steede ◽  
Blake J. Rust ◽  
Mohammad M. Hossain ◽  
Lucy C. Freytag ◽  
James E. Robinson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
B Cell ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Envelope Glycoprotein ◽  
Envelope Glycoprotein Gp120 ◽  
Immunodeficiency Virus ◽  
Glycoprotein Gp120

scholarly journals Neutralizing Antibodies Associated with Viremia Control in a Subset of Individuals after Treatment of Acute Human Immunodeficiency Virus Type 1 Infection

2001 ◽  
Vol 75 (21) ◽  
pp. 10200-10207 ◽  
Author(s):  
David C. Montefiori ◽  
Tanya S. Hill ◽  
Ha T. T. Vo ◽  
Bruce D. Walker ◽  
Eric S. Rosenberg
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cell ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Neutralizing Antibodies ◽  
Neutralizing Antibody ◽  
Treatment Interruption ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Immediate treatment of acute human immunodeficiency virus type 1 (HIV-1) infection has been associated with subsequent control of viremia in a subset of patients after therapy cessation, but the immune responses contributing to control have not been fully defined. Here we examined neutralizing antibodies as a correlate of viremia control following treatment interruption in HIV-1-infected individuals in whom highly active antiretriviral therapy (HAART) was initiated during early seroconversion and who remained on therapy for 1 to 3 years. Immediately following treatment interruption, neutralizing antibodies were undetectable with T-cell-line adapted strains and the autologous primary HIV-1 isolate in seven of nine subjects. Env- and Gag-specific antibodies as measured by enzyme-linked immunosorbent assay were also low or undetectable at this time. Despite this apparent poor maturation of the virus-specific B-cell response during HAART, autologous neutralizing antibodies emerged rapidly and correlated with a spontaneous downregulation in rebound viremia following treatment interruption in three subjects. Control of rebound viremia was seen in other subjects in the absence of detectable neutralizing antibodies. The results indicate that virus-specific B-cell priming occurs despite the early institution of HAART, allowing rapid secondary neutralizing-antibody production following treatment interruption in a subset of individuals. Since early HAART limits viral diversification, we hypothesize that potent neutralizing-antibody responses to autologous virus are able to mature and that in some persons these responses contribute to the control of plasma viremia after treatment cessation.

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