ArticleProceedings of the National Academy of Sciences of the United States of America1993
Human immunodeficiency virus proteins induce the inhibitory cAMP/protein kinase A pathway in normal lymphocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 70 citations in OpenAlex.
- Begomovirus capsid proteins interact with cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase of its whitefly vector and modulate virus retention within its vector.Journal of virology · 2025Article
- Article
- HIV-1 Tat-Mediated Calcium Dysregulation and Neuronal Dysfunction in Vulnerable Brain Regions.Current drug targets · 2016Review
- Molecular Mechanisms for cAMP-Mediated Immunoregulation in T cells - Role of Anchored Protein Kinase A Signaling Units.Frontiers in immunology · 2016Review
- Functional Mechanisms of Treg in the Context of HIV Infection and the Janus Face of Immune Suppression.Frontiers in immunology · 2016Review
- The cAMP Pathway as Therapeutic Target in Autoimmune and Inflammatory Diseases.Frontiers in immunology · 2016Review
- A-kinase anchoring proteins as potential drug targets.British journal of pharmacology · 2012Review
- cAMP during HIV infection: friend or foe?AIDS research and human retroviruses · 2012Review
- Protein kinase A phosphorylation activates Vpr-induced cell cycle arrest during human immunodeficiency virus type 1 infection.Journal of virology · 2010Article
- Reverse Transcriptase and Cellular Factors: Regulators of HIV-1 Reverse Transcription.Viruses · 2009Article
- Macrophage inflammatory protein 1alpha inhibits postentry steps of human immunodeficiency virus type 1 infection via suppression of intracellular cyclic AMP.Journal of virology · 2005Article
- Chronic immune activation associated with chronic helminthic and human immunodeficiency virus infections: role of hyporesponsiveness and anergy.Clinical microbiology reviews · 2004Review
- Mechanism of human immunodeficiency virus-induced complement expression in astrocytes and neurons.Journal of virology · 2002Article
- The use of sequence comparison to detect 'identities' in tRNA genes.Nucleic acids research · 1998Article
- Measles virus modulates human T-cell somatostatin receptors and their coupling to adenylyl cyclase.Journal of virology · 1997Article
- Molecular immunopathogenesis of HIV infection.Genitourinary medicine · 1996Review
- Envelope glycoproteins of human immunodeficiency virus type 1: profound influences on immune functions.Microbiological reviews · 1996Review
- Dysregulation of signal transduction pathways as a potential mechanism of nervous system alterations in HIV-1 gp120 transgenic mice and humans with HIV-1 encephalitis.The Journal of clinical investigation · 1996Article
- Induction of intracellular cAMP by a synthetic retroviral envelope peptide: a possible mechanism of immunopathogenesis in retroviral infections.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- The cytoplasmic domain of CD4 plays a critical role during the early stages of HIV infection in T-cells.The EMBO journal · 1994Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Proliferation of normal T lymphocytes is impaired by human immunodeficiency virus (HIV) proteins. In this paper, we demonstrate important parts of this mechanism. Initially, HIV-induced impairment of proliferation was shown to be an active process involving induction of protein tyrosine kinases in both CD4 and CD8 T cells. Furthermore, the impairment of cell proliferation was demonstrated to be linked to induction of the inhibitory protein kinase A (PKA) pathway by HIV proteins. This induction of PKA was accompanied by an increase in intracellular cAMP, which is necessary for the activation of PKA. Finally, increases in cAMP/PKA activity were shown to induce biochemical changes that impaired proliferation when cells were stimulated with phytohemagglutinin. This was demonstrated by showing that (i) agents, other than HIV proteins, that increase cAMP/PKA activity (cholera toxoid and 8-bromo-cAMP) also decreased T-lymphocyte proliferation; (ii) exposure of lymphocytes to HIV or cholera toxoid led to decreased membrane activity of the proliferation promoter protein kinase C upon stimulation; and (iii) agents that reduced cAMP generation neutralized the effect of HIV proteins and restored lymphocyte proliferation. These studies show that the HIV-induced augmentation of cAMP/PKA activity may be a key part of the mechanism responsible for all or part of the HIV-induced anergy of T lymphocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.