scholarly journals Human immunodeficiency virus type 1 interaction with the membrane of CD4+ cells induces the synthesis and nuclear translocation of 70K heat shock protein

1994 ◽  
Vol 75 (1) ◽  
pp. 193-199 ◽  
Author(s):  
G. Furlini ◽  
M. Vignoli ◽  
M. C. Re ◽  
D. Gibellini ◽  
E. Ramazzotti ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Nuclear Translocation ◽  
Cd4 Cells ◽  
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.

scholarly journals The Protein Tyrosine Kinase p56lck Is Required for Triggering NF-κB Activation upon Interaction of Human Immunodeficiency Virus Type 1 Envelope Glycoprotein gp120 with Cell Surface CD4

1998 ◽  
Vol 72 (7) ◽  
pp. 6207-6214 ◽  
Author(s):  
Laurence Briant ◽  
Véronique Robert-Hebmann ◽  
Claire Acquaviva ◽  
Annegret Pelchen-Matthews ◽  
Mark Marsh ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Nuclear Translocation ◽  
Mutant Form ◽  
Wild Type ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
In Cells

ABSTRACT We have previously shown that NF-κB nuclear translocation can be observed upon human immunodeficiency virus type 1 (HIV-1) binding to cells expressing the wild-type CD4 molecule, but not in cells expressing a truncated form of CD4 that lacks the cytoplasmic domain (M. Benkirane, K.-T. Jeang, and C. Devaux, EMBO J. 13:5559–5569, 1994). This result indicated that the signaling cascade which controls HIV-1-induced NF-κB activation requires the integrity of the CD4 cytoplasmic tail and suggested the involvement of a second protein that binds to this portion of the molecule. Here we investigate the putative role of p56 lck as a possible cellular intermediate in this signal transduction pathway. Using human cervical carcinoma HeLa cells stably expressing CD4, p56 lck , or both molecules, we provide direct evidence that expression of CD4 and p56 lck is required for HIV-1-induced NF-κB translocation. Moreover, the fact that HIV-1 stimulation did not induce nuclear translocation of NF-κB in cells expressing a mutant form of CD4 at position 420 (C420A) and the wild-type p56 lck indicates the requirement for a functional CD4-p56 lck complex.

scholarly journals Evaluation of TruCount Absolute-Count Tubes for Determining CD4 and CD8 Cell Numbers in Human Immunodeficiency Virus-Positive Adults

2000 ◽  
Vol 7 (3) ◽  
pp. 336-343 ◽  
Author(s):  
Carol T. Schnizlein-Bick ◽  
John Spritzler ◽  
Cynthia L. Wilkening ◽  
Janet K. A. Nicholson ◽  
Maurice R. G. O'Gorman
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Cd4 Count ◽  
Cd4 Cells ◽  
Absolute Count ◽  
Individual Site ◽  
Immunodeficiency Virus ◽  
Count Change

ABSTRACT A single-platform technology that uses an internal bead standard and three-color flow cytometry to determine CD4 and CD8 absolute counts was evaluated for reproducibility and agreement. Values obtained using TruCount absolute-count tubes were compared to those obtained using a two-color predicate methodology. Sixty specimens from human immunodeficiency virus type 1-infected donors were shipped to five laboratories. Each site also analyzed replicates of 14 human immunodeficiency virus type 1-infected local specimens at 6 h and again at 24 h. The interlaboratory variability was significantly less with TruCount (median difference in percent coefficient of variation [%CV] between the two methods was −8% and −3% for CD4 and CD8, respectively) than with the predicate method. Intralaboratory variability was smaller, with a median difference in %CV of −1% for both CD4 and CD8 with 6-h samples and −2% and −3% for CD4 and CD8, respectively, with 24-h samples. Use of TruCount for shipped samples resulted in a median CD4 count change of 7 cells (50th estimated percentile) when all laboratories and CD4 strata were combined. For on-site samples, the median CD4 count change was 10 CD4 cells for 6-h samples and 2 CD4 cells for 24-h samples. Individual site biases occurred in both directions and cancelled each other when the data were combined for all laboratories. Thus, the combined data showed a smaller change in median CD4 count than what may have occurred at an individual site. In summary, the use of TruCount decreased both the inter- and intralaboratory variability in determining absolute CD4 and CD8 counts.

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