ArticleJournal of virology2011
Transcriptional repression of C4 complement by hepatitis C virus proteins.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 61 citations in OpenAlex.
- Inhibition of c3 convertase activity by hepatitis C virus as an additional lesion in the regulation of complement components.PloS one · 2014Trial
- Role of CD4+ T cell mannose binding lectin in Schistosoma-induced pulmonary hypertension.JCI insight · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Local complement activation and modulation in mucosal immunity.Mucosal immunology · 2024Review
- Key role of interferon regulatory factor 1 (IRF-1) in regulating liver disease: progress and outlook.Journal of Zhejiang University. Science. B · 2024Review
- Is the central complement component C3 altered in the synergy of HIV infection and preeclampsia?European journal of obstetrics & gynecology and reproductive biology: X · 2023Article
- Metabolomic and Proteomic Profiling of Porcine Intestinal Epithelial Cells Infected with Porcine Epidemic Diarrhea Virus.International journal of molecular sciences · 2023Article
- Role of Hepatitis C Infection in Acute Liver Injury/Acute Liver Failure in North America.Digestive diseases and sciences · 2023Review
- Role of fluid-phase complement system regulation in the development of hepatitis C virus-associated glomerulonephritis.PloS one · 2022Article
- Virus-Encoded Complement Regulators: Current Status.Viruses · 2021Review
- Polysaccharides Extracted FromFrontiers in pharmacology · 2021Article
- Complement C4, Infections, and Autoimmune Diseases.Frontiers in immunology · 2021Review
- Interferon regulatory factor 1 (IRF1) and anti-pathogen innate immune responses.PLoS pathogens · 2021Review
- Interactions of viruses and the humoral innate immune response.Clinical immunology (Orlando, Fla.) · 2020Review
- "Complimenting the Complement": Mechanistic Insights and Opportunities for Therapeutics in Hepatocellular Carcinoma.Frontiers in oncology · 2020Review
- In the Crosshairs: RNA Viruses OR Complement?Frontiers in immunology · 2020Review
- Binding of Free and Immune Complex-Associated Hepatitis C Virus to Erythrocytes Is Mediated by the Complement System.Hepatology (Baltimore, Md.) · 2018Article
- The Complement System and C1q in Chronic Hepatitis C Virus Infection and Mixed Cryoglobulinemia.Frontiers in immunology · 2018Review
- Complement Evasion Strategies of Viruses: An Overview.Frontiers in microbiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The fourth component of human complement (C4) plays an important role in innate immune function. C4 activity has been observed to be significantly lower in patients with chronic hepatitis C virus (HCV) infections, although the mechanism remains unknown. In this study, we have examined the mechanisms of C4 regulation by HCV. Liver biopsy specimens from patients with chronic HCV infections displayed significantly lower C4 mRNA levels than liver tissue samples from patients with unrelated liver disease. Further, C4 mRNA levels of the two isoforms (C4A and C4B) were significantly reduced in hepatocytes transfected with RNA from HCV genotype 1a or 2a. Subsequently, a significant C4 regulatory role of HCV core or NS5A upon C4 promoter activity was observed. HCV core or NS5A transgenic mice displayed a reduction in C4 mRNA. Gamma interferon (IFN-γ)-induced C4 promoter activation was also impaired in the presence of HCV proteins. We further demonstrated that HCV core reduced the expression of upstream stimulating factor 1 (USF-1), a transcription factor important for basal C4 expression. On the other hand, the expression of interferon regulatory factor 1 (IRF-1), which is important for IFN-γ-induced C4 expression, was inhibited by hepatocytes expressing HCV NS5A. These results underscore the roles of HCV proteins in innate immune regulation in establishing a chronic infection.
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What OpenQuestion holds
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.