ReviewWorld journal of gastroenterology2007
The interferon inducing pathways and the hepatitis C virus.
Review in World journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 45 citations in OpenAlex.
- Micronutrients and bioactive substances: Their potential roles in combating COVID-19.Nutrition (Burbank, Los Angeles County, Calif.) · 2021Review
- In search of drugs to alleviate suppression of the host's innate immune responses against SARS-CoV-2 using a molecular modeling approach.In silico pharmacology · 2021Article
- HCV and flaviviruses hijack cellular mechanisms for nuclear STAT2 degradation: Up-regulation of PDLIM2 suppresses the innate immune response.PLoS pathogens · 2019Article
- Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ.Immunobiology · 2019Article
- MicroRNA Profile of HCV Spontaneous Clarified Individuals, Denotes Previous HCV Infection.Journal of clinical medicine · 2019Article
- Article
- Response of hepatitis C virus to long-term passage in the presence of alpha interferon: multiple mutations and a common phenotype.Journal of virology · 2013Article
- Inhibition of HCV by the serpin antithrombin III.Virology journal · 2012Article
- Review of boceprevir and telaprevir for the treatment of chronic hepatitis C.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2012Review
- Article
- Natural killer cell functional dichotomy: a feature of chronic viral hepatitis?Frontiers in immunology · 2012Article
- High plasma interleukin-18 levels mark the acute phase of hepatitis C virus infection.The Journal of infectious diseases · 2011Article
- Interferons as therapeutic agents for infectious diseases.Infectious disease clinics of North America · 2011Review
- Possible association of VISA gene polymorphisms with susceptibility to systemic lupus erythematosus in Chinese population.Molecular biology reports · 2011Article
- Expression of an IRF-3 fusion protein and mouse estrogen receptor, inhibits hepatitis C viral replication in RIG-I-deficient Huh 7.5 cells.Virology journal · 2011Article
- Core as a novel viral target for hepatitis C drugs.Viruses · 2010Article
- Function and regulation of retinoic acid-inducible gene-I.Critical reviews in immunology · 2010Review
- Enhanced anti-HCV activity of interferon alpha 17 subtype.Virology journal · 2009Article
- Common variants in immune and DNA repair genes and risk for human papillomavirus persistence and progression to cervical cancer.The Journal of infectious diseases · 2009Article
- Inhibition of HBV gene expression and replication by stably expressed interferon-alpha1 via adeno-associated viral vectors.The journal of gene medicine · 2008Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune response is triggered by a variety of pathogens, including viruses, and requires rapid induction of type I interferons (IFN), such as IFNbeta and IFNalpha. IFN induction occurs when specific pathogen motifs bind to specific cellular receptors. In non-professional immune, virally-infected cells, IFN induction is essentially initiated after the binding of dsRNA structures to TLR3 receptors or to intracytosolic RNA helicases, such as RIG-I/MDA5. This leads to the recruitment of specific adaptors, such as TRIF for TLR3 and the mitochondrial-associated IPS-1/VISA/MAVS/CARDIF adapter protein for the RNA helicases, and the ultimate recruitment of kinases, such as MAPKs, the canonical IKK complex and the TBK1/IKKepsilon kinases, which activate the transcription factors ATF-2/c-jun, NF-kappaB and IRF3, respectively. The coordinated action of these transcription factors leads to induction of IFN and of pro-inflammatory cytokines and to the establishment of the innate immune response. HCV can cleave both the adapters TRIF and IPS-1/VISA/MAVS/CARDIF through the action of its NS3/4A protease. This provokes abrogation of the induction of the IFN and cytokine pathways and favours viral propagation and presumably HCV chronic infection.
Indexed as
Identifiers
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.