ArticleJournal of virology2011
Adenovirus type 5 rupture of lysosomes leads to cathepsin B-dependent mitochondrial stress and production of reactive oxygen species.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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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.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Targeting respiratory virus-induced reactive oxygen species in airways diseases.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- GAPDH suppresses adenovirus-induced oxidative stress and enables a superfast production of recombinant adenovirus.Genes & diseases · 2024Article
- The HN protein of Newcastle disease virus induces cell apoptosis through the induction of lysosomal membrane permeabilization.PLoS pathogens · 2024Article
- Anastrozole Protects against Human Coronavirus Infection by Ameliorating the Reactive Oxygen Species-Mediated Inflammatory Response.Antioxidants (Basel, Switzerland) · 2024Article
- Activation of the NLRP3 inflammasome by human adenovirus type 7 L4 100-kilodalton protein.Frontiers in immunology · 2024Article
- DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus.Virology journal · 2023Review
- The Interplay between Viruses and Host DNA Sensors.Viruses · 2022Review
- STING signaling activation inhibits HBV replication and attenuates the severity of liver injury and HBV-induced fibrosis.Cellular & molecular immunology · 2022Article
- "Repair Me if You Can": Membrane Damage, Response, and Control from the Viral Perspective.Cells · 2020Review
- Inhibitory effects of piceatannol on human cytomegalovirus (hCMV) in vitro.Journal of microbiology (Seoul, Korea) · 2020Article
- Innate Immune Sensing of Influenza A Virus.Viruses · 2020Review
- Adeno-associated viral vector-mediated immune responses: Understanding barriers to gene delivery.Pharmacology & therapeutics · 2020Review
- NOD-like Receptors in the Eye: Uncovering Its Role in Diabetic Retinopathy.International journal of molecular sciences · 2020Review
- HLA class II antibodies induce necrotic cell death in human endothelial cells via a lysosomal membrane permeabilization-mediated pathway.Cell death & disease · 2019Article
- Inhibition of type I interferon responses by adenovirus serotype-dependent Gas6 binding.Virology · 2018Article
- Repositioning of the β-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome.Frontiers in immunology · 2018Article
- Regulation of type I interferon responses by mitochondria-derived reactive oxygen species in plasmacytoid dendritic cells.Redox biology · 2017Article
- The Immune Response to Astrovirus Infection.Viruses · 2016Review
- Adenovirus sensing by the immune system.Current opinion in virology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In response to viral infection, reactive oxygen species (ROS) mediate innate immune signaling or generate danger signals to activate immune cells. The mechanisms of virally induced ROS are poorly defined, however. We demonstrate that ROS are produced within minutes of adenovirus type 5 (Ad5) infection of macrophages and that oxidative stress supports Ad5-induced cytokine secretion. We show that short hairpin RNA (shRNA) knockdown of TLR9 has no effect on ROS production despite observed decreases in Ad-induced cytokine secretion. A major source of ROS in macrophages is NADPH oxidase. However, shRNA knockdown of the NADPH oxidase subunit NOX2 does not attenuate Ad-induced ROS. Induction of ROS is not observed in cells infected with a temperature-sensitive mutant of Ad2, ts1, which is defective in endosomal membrane penetration during cell entry. Further, Ad5, but not ts1, induces the release of lysosomal cathepsin B into the cytoplasm of infected cells. In agreement with this finding, we observe a loss of mitochondrial membrane potential upon Ad infection which requires Ad endosomal membrane penetration and cathepsin B activity. Overexpression of Bcl-2 attenuates Ad5-induced ROS, further supporting the role for mitochondrial membrane destabilization as the source of ROS in response to Ad5 infection. Together, these data suggest that ROS produced in response to Ad5 infection depends on the virally induced endosomal membrane rupture to release lysosomal cathepsins. Furthermore, the release of cathepsins leads to mitochondrial membrane disruption and thus the release of ROS from the mitochondria.
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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.