ArticleJournal of virology2012
Hepatitis C virus-induced autophagy is independent of the unfolded protein response.
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 35 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
35 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- Autophagy in HCV Replication and Protein Trafficking.International journal of molecular sciences · 2021Review
- Nonstructural protein 6 of porcine epidemic diarrhea virus induces autophagy to promote viral replication via the PI3K/Akt/mTOR axis.Veterinary microbiology · 2020Article
- Article
- Crosstalk between RNA Metabolism and Cellular Stress Responses during Zika Virus Replication.Pathogens (Basel, Switzerland) · 2020Review
- Singapore Grouper Iridovirus (SGIV) Inhibited Autophagy for Efficient Viral Replication.Frontiers in microbiology · 2020Article
- Role of autophagy during the replication and pathogenesis of common mosquito-borne flavi- and alphaviruses.Open biology · 2019Review
- Diverse Functions of Autophagy in Liver Physiology and Liver Diseases.International journal of molecular sciences · 2019Review
- Transmembrane Protein 39A Promotes the Replication of Encephalomyocarditis VirusFrontiers in microbiology · 2019Article
- The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions.International journal of molecular sciences · 2018Review
- Subversion of cellular autophagy during virus infection: Insights from hepatitis B and hepatitis C viruses.Liver research (Beijing, China) · 2018Article
- Hepatitis C virus: Morphogenesis, infection and therapy.World journal of hepatology · 2018Review
- Dengue virus-induced ER stress is required for autophagy activation, viral replication, and pathogenesis both in vitro and in vivo.Scientific reports · 2018Article
- Article
- The amino-terminus of the hepatitis C virus (HCV) p7 viroporin and its cleavage from glycoprotein E2-p7 precursor determine specific infectivity and secretion levels of HCV particle types.PLoS pathogens · 2017Article
- The autophagy elongation complex (ATG5-12/16L1) positively regulates HCV replication and is required for wild-type membranous web formation.Scientific reports · 2017Article
- Anti-hepatitis C virus potency of a new autophagy inhibitor using human liver slices model.World journal of hepatology · 2016Article
- Hepatitis C Virus Infection Induces Autophagy as a Prosurvival Mechanism to Alleviate Hepatic ER-Stress Response.Viruses · 2016Review
- Membrane dynamics associated with viral infection.Reviews in medical virology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatitis C virus (HCV) has been shown to induce autophagy and the unfolded protein response (UPR), but the mechanistic link between the induction of these two cellular processes remains unclear. We demonstrate here that HCV infection induces autophagy, as judged by accumulation of lipidated LC3-II, and that this induction occurs rapidly after infection, preceding the stimulation of the UPR, which occurs only at later stages, after the viral envelope glycoproteins have been expressed to high levels. Furthermore, both genotype 1b and 2a subgenomic replicons expressing nonstructural (NS3-5B) proteins and JFH-1 virus lacking the envelope glycoproteins potently induced autophagy in the absence of detectable UPR. This ability was also shared by a subgenomic replicon derived from the related GB virus B (GBV-B). We also show that small interfering RNA (siRNA)-mediated silencing of the key UPR inducer, Ire1, has no effect on HCV genome replication or the induction of autophagy, further demonstrating that the UPR is not required for these processes. Lastly, we demonstrate that the HCV replicase does not colocalize with autophagosomes, suggesting that the induction of autophagy is not required to generate the membrane platform for HCV RNA replication.
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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.