ReviewCells2018
Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion.
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Identity by descent and local ancestry mapping of HCV spontaneous clearance in populations of diverse ancestries.BMC genomics · 2025Article
- Gut Microbiota and Cardiovascular Diseases: Unraveling the Role of Dysbiosis and Microbial Metabolites.International journal of molecular sciences · 2025Review
- Mcl-1 Protein and Viral Infections: A Narrative Review.International journal of molecular sciences · 2024Review
- Identification of TREM2-positive tumor-associated macrophages in esophageal squamous cell carcinoma: implication for poor prognosis and immunotherapy modulation.Frontiers in immunology · 2023Article
- Evaluation of interactions between the hepatitis C virus NS3/4A and sulfonamidobenzamide based molecules using molecular docking, molecular dynamics simulations and binding free energy calculations.Journal of computer-aided molecular design · 2023Article
- Alterations of the gut microbiota associated with the occurrence and progression of viral hepatitis.Frontiers in cellular and infection microbiology · 2023Article
- Identification of a cytokine-dominated immunosuppressive class in squamous cell lung carcinoma with implications for immunotherapy resistance.Genome medicine · 2022Article
- SARS-CoV-2 Infection: A Possible Risk Factor for Incidence and Recurrence of Cancers.International journal of hematology-oncology and stem cell research · 2022Review
- High Levels of CD244 Rather Than CD160 Associate With CD8Frontiers in immunology · 2022Article
- Inflammation response and liver stiffness: predictive model of regression of hepatic stiffness after sustained virological response in cirrhotics patients with chronic hepatitis C.Clinical and experimental medicine · 2021Article
- Dysregulation of the immune response in coronavirus disease 2019.Cell biology international · 2021Review
- Lymphopenia in COVID-19: Therapeutic opportunities.Cell biology international · 2020Review
- A bioinformatics investigation into the pharmacological mechanisms of the effect of the Yinchenhao decoction on hepatitis C based on network pharmacology.BMC complementary medicine and therapies · 2020Article
- Microrna-130a Downregulates HCV Replication through an atg5-Dependent Autophagy Pathway.Cells · 2019Article
- Topological DNA damage, telomere attrition and T cell senescence during chronic viral infections.Immunity & ageing : I & A · 2019Article
- T-Cell Exhaustion in Chronic Infections: Reversing the State of Exhaustion and Reinvigorating Optimal Protective Immune Responses.Frontiers in immunology · 2018Review
- The Sero-Prevalence of Hepatitis B and C Viruses in Municipal Waste Collectors in Southwest of Iran.Indian journal of occupational and environmental medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) represents a challenging global health threat to ~200 million infected individuals. Clinical data suggest that only ~10⁻15% of acutely HCV-infected individuals will achieve spontaneous viral clearance despite exuberant virus-specific immune responses, which is largely attributed to difficulties in recognizing the pathognomonic symptoms during the initial stages of exposure to the virus. Given the paucity of a suitable small animal model, it is also equally challenging to study the early phases of viral establishment. Further, the host factors contributing to HCV chronicity in a vast majority of acutely HCV-infected individuals largely remain unexplored. The last few years have witnessed a surge in studies showing that HCV adopts myriad mechanisms to disconcert virus-specific immune responses in the host to establish persistence, which includes, but is not limited to viral escape mutations, viral growth at privileged sites, and antagonism. Here we discuss a few hitherto poorly explained mechanisms employed by HCV that are believed to lead to chronicity in infected individuals. A better understanding of these mechanisms would aid the design of improved therapeutic targets against viral establishment in susceptible individuals.
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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.