ArticleJournal of virology2012
Hepatitis C virus proteins inhibit C3 complement production.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
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Who cites it
50 citing papers in PubMed, 86 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
- Mechanistic insight into complement C3 regulation during chronic HBV infection: effect on viral persistence and host immune response.Journal of biomedical science · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Lnc-DARVR/miR-365-1-5p/LAMB1 axis regulates rotavirus replication via the complement C3 pathway.Journal of virology · 2025Article
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Mapping the interaction sites of human and avian influenza A viruses and complement factor H.Frontiers in immunology · 2024Article
- Zika Virus Infection Induces Interleukin-1β-Mediated Inflammatory Responses by Macrophages in the Brain of an Adult Mouse Model.Journal of virology · 2023Article
- How much (evil) intelligence can be encoded by 30 kb?Biologia futura · 2023Article
- Role of Hepatitis C Infection in Acute Liver Injury/Acute Liver Failure in North America.Digestive diseases and sciences · 2023Review
- Nonstructural Protein 1 of Variant PEDV Plays a Key Role in Escaping Replication Restriction by Complement C3.Journal of virology · 2022Article
- Article
- Serum cystatin C is an early renal dysfunction biomarker in patients with hepatitis C virus.Egyptian liver journal · 2022Article
- Role of fluid-phase complement system regulation in the development of hepatitis C virus-associated glomerulonephritis.PloS one · 2022Article
- Hepatitis C Virus Evades Interferon Signaling by Suppressing Long Noncoding RNA Linc-Pint Involving C/EBP-β.Journal of virology · 2021Article
- Cerebral Organoids Derived from a Parkinson's Patient Exhibit Unique Pathogenesis from Chikungunya Virus Infection When Compared to a Non-Parkinson's Patient.Pathogens (Basel, Switzerland) · 2021Article
- Interactive Impacts from Hepatitis C Virus Infection and Mixed Cryoglobulinemia on Complement Levels.Digestive diseases and sciences · 2021Article
- Virus-Encoded Complement Regulators: Current Status.Viruses · 2021Review
- Interactions of viruses and the humoral innate immune response.Clinical immunology (Orlando, Fla.) · 2020Review
- In the Crosshairs: RNA Viruses OR Complement?Frontiers in immunology · 2020Review
- Repression of MicroRNA-30e by Hepatitis C Virus Enhances Fatty Acid Synthesis.Hepatology communications · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The third component of human complement (C3) plays a central role in innate immune function as its activation is required to trigger classical as well as alternative complement pathways. In this study, we have observed that sera from patients chronically infected with hepatitis C virus (HCV) displayed significantly lower C3 levels than sera from healthy individuals. Liver biopsy specimens from the same patients also exhibited lower C3 mRNA expression than liver tissues from healthy donors. C3 mRNA level was reduced in hepatocytes upon infection with cell culture-grown HCV genotype 1a or 2a in vitro. Further analysis suggested that HCV core protein displayed a weak repression of C3 promoter activity by downregulating the transcription factor farnesoid X receptor (FXR). On the other hand, HCV NS5A protein strongly downregulated C3 promoter activity at the basal level or in the presence of interleukin-1β (IL-1β) as an inducer. In addition, the expression of the transcription factor CAAT/enhancer binding protein beta (C/EBP-β), which binds to the IL-1/IL-6 response element in the C3 promoter, was inhibited in liver biopsy specimens. Furthermore, expression of C/EBP-β was reduced in hepatocytes infected with cell culture-grown HCV, as well as in hepatocytes transfected with the NS5A genomic region of HCV. Together, these results underscore the role of HCV NS5A protein in impairing innate immune function.
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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.