ReviewFrontiers in microbiology2014
Unfolded protein response in hepatitis C virus infection.
Review in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 68 citations in OpenAlex.
- Hepatitis C Virus Enhances Lysosome-Associated Membrane Protein 2 A Transcription Through Nuclear Factor Erythroid 2-Related Factor 2 to Support Viral Replication.Microbiology and immunology · 2026Article
- Glutamine-Linked Cellular Stress Responses in Viral Infection: Mechanisms, Crosstalk, and Future Perspectives.International journal of molecular sciences · 2026Review
- Pseudorabies virus infection induces lymphocyte depletion associated with cellular apoptosis and endoplasmic reticulum stress in the mouse spleen.BMC veterinary research · 2025Article
- Emerging role of natural killer cells in non-AIDS comorbidities during suppressive antiretroviral therapy.Current opinion in HIV and AIDS · 2025Review
- Innate Immune Response to Viral Infection.Advances in experimental medicine and biology · 2025Review
- ATF6 Promotes Colorectal Cancer Growth and Stemness by Regulating the Wnt Pathway.Cancer research communications · 2024Article
- The cGAS-STING pathway in viral infections: a promising link between inflammation, oxidative stress and autophagy.Frontiers in immunology · 2024Review
- Uncloaking the viral glycocalyx: How do viruses exploit glycoimmune checkpoints?Advances in virus research · 2024Review
- Unfolded protein response is involved in resistance to Neospora caninum infection via IRE1α-XBP1s-NOD2 Axis.Parasitology research · 2023Article
- Screening core genes and signaling pathways after SFTSV infection by integrated transcriptome profiling analysis.Virus research · 2023Article
- Endoplasmic Reticulum Stress in Elderly Patients with COVID-19: Potential of Melatonin Treatment.Viruses · 2023Review
- The H protein of attenuated canine distemper virus is degraded via endoplasmic reticulum-associated protein degradation.Frontiers in veterinary science · 2023Article
- Endoplasmic reticulum stress-mediated cell death in liver injury.Cell death & disease · 2022Review
- Review
- Pharmacological Manipulation of UPR: Potential Antiviral Strategy Against Chikungunya Virus.Indian journal of microbiology · 2022Article
- Review
- Activation of the CaViruses · 2022Article
- The HCV Envelope Glycoprotein Down-Modulates NF-κB Signalling and Associates With Stimulation of the Host Endoplasmic Reticulum Stress Pathway.Frontiers in immunology · 2022Article
- Article
- Evidence of Transcriptional Shutoff by Pathogenic Viral Haemorrhagic Septicaemia Virus in Rainbow Trout.Viruses · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Hepatitis C virus (HCV) is a single-stranded, positive-sense RNA virus of clinical importance. The virus establishes a chronic infection and can progress from chronic hepatitis, steatosis to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The mechanisms of viral persistence and pathogenesis are poorly understood. Recently the unfolded protein response (UPR), a cellular homeostatic response to endoplasmic reticulum (ER) stress, has emerged to be a major contributing factor in many human diseases. It is also evident that viruses interact with the host UPR in many different ways and the outcome could be pro-viral, anti-viral or pathogenic, depending on the particular type of infection. Here we present evidence for the elicitation of chronic ER stress in HCV infection. We analyze the UPR signaling pathways involved in HCV infection, the various levels of UPR regulation by different viral proteins and finally, we propose several mechanisms by which the virus provokes the UPR.
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.