ArticleThe Journal of infectious diseases2011
High plasma interleukin-18 levels mark the acute phase of hepatitis C virus infection.
Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Association of elevated serum active IL-18 levels with cytokine profiles and clinical features in adult-onset still's disease.Frontiers in immunology · 2026Article
- The inflammasome next door: characterizing pyroptosis induction in HCV-infected and uninfected bystander cellsFrontiers in cellular and infection microbiology · 2025Article
- Biomarkers in Detection of Hepatitis C Virus Infection.Pathogens (Basel, Switzerland) · 2024Review
- Advances in the mechanism of inflammasomes activation in herpes virus infection.Frontiers in immunology · 2024Review
- Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.Viruses · 2022Review
- Long-Lasting Imprint in the Soluble Inflammatory Milieu Despite Early Treatment of Acute Symptomatic Hepatitis C.The Journal of infectious diseases · 2022Article
- Review
- Differential Cytokine Signatures of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and Influenza Infection Highlight Key Differences in Pathobiology.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Article
- Article
- Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death.Frontiers in immunology · 2022Article
- Interleukin-18 and tumor necrosis factor-α are elevated in solid organ transplant recipients with possible cytomegalovirus end-organ disease.Transplant infectious disease : an official journal of the Transplantation Society · 2021Article
- Review
- Innate Immunity in Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2021Review
- NLRP3 Inflammasome Expression in Gingival Crevicular Fluid of Patients with Periodontitis and Chronic Hepatitis C.Mediators of inflammation · 2021Article
- Inflammasome genes polymorphisms may influence the development of hepatitis C in the Amazonas, Brazil.PloS one · 2021Article
- Review
- Modulation of calcium signaling pathway by hepatitis C virus core protein stimulates NLRP3 inflammasome activation.PLoS pathogens · 2019Article
- Human immunodeficiency virus and liver disease: A comprehensive update.Hepatology communications · 2017Article
- Dose of Retroviral Infection Determines Induction of Antiviral NK Cell Responses.Journal of virology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundProinflammatory cytokines play a critical role in antiviral immune responses. Large-scale genome studies have found correlations between single-nucleotide polymorphisms (SNPs) in the interleukin (IL) 18 promoter and spontaneous control of hepatitis C virus (HCV), suggesting a role in clearance.
methodsPlasma IL-18, IL-1β, IL-6, IL-8, IL-12, interferon-γ, tumor necrosis factor-α, alanine aminotransferase (ALT), and HCV RNA levels were assessed longitudinally in subjects with known dates of HCV acquisition and analyzed according to IL-18 SNPs and outcome, either spontaneous clearance (SC) (n = 13) or persistent infection (PI) (n = 25).
resultsNo significant change in plasma proinflammatory cytokine expression was observed with the exception of IL-18, which increased in every subject with initial detection of HCV RNA. In every SC subject, IL-18 returned to the preinfection baseline concomitant with HCV control. In PI subjects, IL-18 declined following the acute phase of infection but remained above the preinfection baseline throughout chronic infection and did not correlate with HCV RNA or ALT levels.
conclusionsPlasma IL-18 was an early and the most reliably detected host response to HCV infection measured in blood. Reduced IL-18 production with transition to chronic infection without correlation with HCV RNA or ALT levels suggests modulation of the innate response with persistent infection.
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