Human immunodeficiency virus induces phosphorylation of its cell surface receptor

@article{Fields1988HumanIV,
  title={Human immunodeficiency virus induces phosphorylation of its cell surface receptor},
  author={Alan P. Fields and Daniel P. Bednarik and Allan D. Hess and William Stratford May},
  journal={Nature},
  year={1988},
  volume={333},
  pages={278-280}
}
AIDS is an immunoregulatory disorder characterized by depletion of the CD4+, helper/inducer lymphocyte population1. The causative agent of this disease is the human immunodeficiency virus, HIV2–4, which infects CD4+ cells and leads to cytopathic effects characterized by syncytia formation and cell death5,6. Recent studies have demonstrated that binding of HIV to its cellular receptor CD4 is necessary for viral entry7,8. We find that binding of HIV to CD4 induces rapid and sustained… 

Envelope glycoproteins of human immunodeficiency virus type 1: profound influences on immune functions.

This review summarizes work done by several investigators demonstrating the profound biological effects of envelope glycoproteins of HIV-1 on immune system cells, which include effects on differentiation of CD34+ lymphoid progenitor cells and thymocytes, aberrant activation and cytokine secretion patterns of mature T cells, induction of apoptosis, B-cell hyperactivity, inhibition of T-cell dependent B-cells, and effects on neuronal cells.

Envelope glycoproteins of human immunodeficiency virus type 1: profound influences on immune functions

This review summarizes work done by several investigators demonstrating the profound biological effects of envelope glycoproteins of HIV-1 on immune system cells, which include effects on differentiation of CD34+ lymphoid progenitor cells and thymocytes, aberrant activation and cytokine secretion patterns of mature T cells, induction of apoptosis, B-cell hyperactivity, inhibition of T-cell dependent B-cells, and effects on neuronal cells.

HIV-1 binding to CD4 T cells does not induce a Ca2+ influx or lead to activation of protein kinases.

It is found that Ca2+ influx was not induced by the binding of HIV to CD4+ cells, and the phosphorylation state of the CD4 molecule was examined by radioimmunoprecipitation and found to be unaltered by thebinding of HIV under conditions in which TPA induced rapid CD4 phosphorylated.

Synergism between HIV gp120 and gp120-specific antibody in blocking human T cell activation.

Experimental findings reported here indicate that CD4-bound gp120 attracts gp120-specific antibodies derived from the blood of HIV-seropositive individuals to form a trimolecular complex with itself and CD4 that suppresses the activation of T cells as measured by mobilization of intracellular calcium (Ca2i+).

Mechanism of HIV-1 entry into CD4+ T cells.

In the absence of T cell stimuli, resting CD4+ cells are resistant to HIV-1 entry, which may explain the observation that at any given time the vast majority ofCD4+ T cells in HIV- 1 seropositive patients are not infected despite the presence of relatively large quantities of free virus in the blood of such patients.

The human immunodeficiency virus type 1 (HIV-1) CD4 receptor and its central role in promotion of HIV-1 infection.

The mechanisms leading to CD4 downmodulation by HIV-1 are multiple and complex; these include degradation of CD4 by Vpu, formation of intracellular complexes between CD4 and the envelope precursor gp160, and internalization by the Nef protein.

Infection of B lymphocytes by the human immunodeficiency virus and their susceptibility to cytotoxic cells

Two cell lines, a B lymphoblastoid cell line and a glial cell line derived from human embryonal brain tissue, are productively infectable with two distinct isolates of HIV as judged by electron microscopy and immunological and virological studies.

Understanding the CD4 molecule: Surface expression and function

Selective CD4 modulations have independently redefined the specific contributions ofCD4 surface expression during T cell activation and may establish a role for CD4 receptor subtypes during HIV‐1 infenction of CD4+ cells.

Mechanisms and Specificity of HIV Entry into Host Cells

  • N. Düzgüneş
  • Biology, Medicine
    Advances in Experimental Medicine and Biology
  • 1991
The role of CD4 in the Penetration of Cells by HIV and the Assembly of the HIV-1 Env Glycoprotein into Dimers and Tetramers are studied.
...

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