ArticleJournal of virology2011
Human cytomegalovirus induces multiple means to combat 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 39 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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Oxidative stress, inflammation, and apoptosis in Alzheimer's disease associated with HSV-1 and CMV coinfection.Virology journal · 2025Trial
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- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
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- Shrimp Virus Regulates ROS Dynamics via the Nrf2 Pathway to Facilitate Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis.Journal of virology · 2025Article
- Complex roles for proliferating cell nuclear antigen in restricting human cytomegalovirus replication.bioRxiv : the preprint server for biology · 2025Article
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Article
- Review
- DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus.Virology journal · 2023Review
- Poxviruses package viral redox proteins in lateral bodies and modulate the host oxidative response.PLoS pathogens · 2022Article
- Infectious spleen and kidney necrosis virus induces the reactive oxidative species/Nrf2-mediated oxidative stress response for the regulation of mitochondrion-mediated Bax/Bak cell death signals in GF-1 cells.Frontiers in microbiology · 2022Article
- Virus-induced FoxO factor facilitates replication of human cytomegalovirus.Archives of virology · 2022Article
- Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection.Life (Basel, Switzerland) · 2021Review
- Infections at the nexus of metabolic-associated fatty liver disease.Archives of toxicology · 2021Review
- Effect of Reactive Oxygen Species on the Endoplasmic Reticulum and Mitochondria during Intracellular Pathogen Infection of Mammalian Cells.Antioxidants (Basel, Switzerland) · 2021Review
- Nitric Oxide Circumvents Virus-Mediated Metabolic Regulation during Human Cytomegalovirus Infection.mBio · 2020Article
- Host Mitochondrial Requirements of Cytomegalovirus Replication.Current clinical microbiology reports · 2020Article
- Inhibitory effects of piceatannol on human cytomegalovirus (hCMV) in vitro.Journal of microbiology (Seoul, Korea) · 2020Article
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
Reactive oxygen species (ROS) are generated as by-products of many cellular processes and can modulate cellular signaling pathways. However, high ROS levels are toxic; thus, intracellular ROS need to be tightly controlled. Therefore, cells use a group of antioxidant molecules and detoxifying enzymes that remove or detoxify reactive species. We found that the level of the antioxidant glutathione is greatly increased in human cytomegalovirus (HCMV)-infected cells due to activation of glutathione synthetic enzymes. In addition, our data suggest that virus-specific mechanisms are used to induce the expression of target antioxidant and detoxifying enzymes critical for the success of the infection. As a result of this virus-induced anti-ROS environment, key signaling kinases, such as the mammalian target of rapamycin (mTOR) kinase in mTOR complex 1 (mTORC1), are protected from inhibition by exogenous hydrogen peroxide (H(2)O(2)). In this regard, we found that phosphorylation of mTOR kinase at serine 2448 (suggested to be activating) was maintained during infection even under ROS stress conditions that inhibited it in uninfected cells. We also show that AMP-dependent kinase (AMPK)-mediated phosphorylation of serine 792 of raptor, the specificity subunit of mTORC1, increases in infected cells after H(2)O(2) treatment. This phosphorylation is normally inhibitory for mTORC1. However, in infected cells this did not result in inhibition of mTORC1 activity, suggesting that inhibitory effects of raptor phosphorylation are circumvented. Overall, our data suggest that HCMV utilizes virus-specific mechanisms to activate a variety of means to protect the cell and mTORC1 from the effects of ROS.
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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.