ArticleJournal of virology2001
Transcriptional activation of the interleukin-2 promoter by hepatitis C virus core protein.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 69 citations in OpenAlex.
- Article
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- Activation of the CaViruses · 2022Article
- Calcium Ions Signaling: Targets for Attack and Utilization by Viruses.Frontiers in microbiology · 2022Review
- Article
- HCV-coinfection is related to an increased HIV-1 reservoir size in cART-treated HIV patients: a cross-sectional study.Scientific reports · 2019Article
- Article
- Ultrastructural Localization and Molecular Associations of HCV Capsid Protein in Jurkat T Cells.Frontiers in microbiology · 2017Article
- Antiviral Activity of a Novel Compound CW-33 against Japanese Encephalitis Virus through Inhibiting Intracellular Calcium Overload.International journal of molecular sciences · 2016Article
- CD4+ primary T cells expressing HCV-core protein upregulate Foxp3 and IL-10, suppressing CD4 and CD8 T cells.PloS one · 2014Article
- Direct effects of hepatitis C virus on the lymphoid cells.World journal of gastroenterology · 2013Review
- Phenotypic and functional alterations of primary human PBMCs induced by HCV non-enveloped capsid-like particles uptake.Cellular and molecular life sciences : CMLS · 2013Article
- Biological significance of HCV in various kinds of lymphoid cells.International journal of microbiology · 2012Article
- Modulation of IL-2 expression after uptake of hepatitis C virus non-enveloped capsid-like particles: the role of p38 kinase.Cellular and molecular life sciences : CMLS · 2011Article
- Oncogenic potential of hepatitis C virus proteins.Viruses · 2010Article
- Specific activation of 2'-5'oligoadenylate synthetase gene promoter by hepatitis C virus-core protein: a potential for developing hepatitis C virus targeting gene therapy.World journal of gastroenterology · 2009Article
- Viral calciomics: interplays between Ca2+ and virus.Cell calcium · 2009Review
- Viral modulation of T-cell receptor signaling.Journal of virology · 2008Review
- Hepatitis C virus non-structural 5A protein can enhance full-length core protein-induced nuclear factor-kappaB activation.World journal of gastroenterology · 2005Article
- Hepatitis C virus core protein induces an anergic state characterized by decreased interleukin-2 production and perturbation of mitogen-activated protein kinase responses.Journal of virology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Most patients infected with hepatitis C virus (HCV) become chronic carriers. Viruses that efficiently establish persistent infections must have effective ways of evading host defenses. In the case of HCV, little is known about how chronic infections are established or maintained. Besides hepatocytes, several reports suggest that HCV can infect T and B lymphocytes. Since T cells are essential for viral clearance, direct or indirect effects of HCV on T-cell function could influence the outcome of infection. Given that T-cell growth and differentiation require the cytokine interleukin 2 (IL-2), we asked whether HCV might modulate synthesis of IL-2. Portions of the HCV polyprotein were expressed in Jurkat cells under a variety of conditions. We found that the highly conserved HCV core protein, in combination with other stimuli, was able to dramatically activate transcription from the IL-2 promoter. The carboxy-terminal hydrophobic portion of the core protein was required for this activity. Activation was dependent on nuclear factor of activated T cells (NFAT), occurred in cells deficient in the tyrosine kinase p56(lck), and could be blocked by addition of cyclosporin A and by depletion of calcium. These results suggest that the HCV core protein can activate transcription of the IL-2 promoter through the NFAT pathway. This novel activity may have consequences for T-cell development and establishment of persistent infections.
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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.