ArticleJournal of virology2005
Production of infectious human cytomegalovirus virions is inhibited by drugs that disrupt calcium homeostasis in the endoplasmic reticulum.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Infection-induced peripheral mitochondria fission drives ER encapsulations and inter-mitochondria contacts that rescue bioenergetics.Nature communications · 2024Article
- Opposite Effects of Apoptotic and Necroptotic Cellular Pathways on Rotavirus Replication.Journal of virology · 2022Article
- Effect of Denervation on XBP1 in Skeletal Muscle and the Neuromuscular Junction.International journal of molecular sciences · 2021Article
- Confounding Roles of ER Stress and the Unfolded Protein Response in Skeletal Muscle Atrophy.International journal of molecular sciences · 2021Review
- The Role of Molecular Chaperones in Virus Infection and Implications for Understanding and Treating COVID-19.Journal of clinical medicine · 2020Review
- P2Y2 purinergic receptor modulates virus yield, calcium homeostasis, and cell motility in human cytomegalovirus-infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human Cytomegalovirus Disruption of Calcium Signaling in Neural Progenitor Cells and Organoids.Journal of virology · 2019Article
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
- Emerging roles of ER stress and unfolded protein response pathways in skeletal muscle health and disease.Journal of cellular physiology · 2018Review
- Targeting Metabolic Reprogramming by Influenza Infection for Therapeutic Intervention.Cell reports · 2017Article
- ATF6α regulates morphological changes associated with senescence in human fibroblasts.Oncotarget · 2016Article
- Review
- Human Cytomegalovirus pTRS1 and pIRS1 Antagonize Protein Kinase R To Facilitate Virus Replication.Journal of virology · 2016Article
- HIV-1 Gag Blocks Selenite-Induced Stress Granule Assembly by Altering the mRNA Cap-Binding Complex.mBio · 2016Article
- Human cytomegalovirus TRS1 protein associates with the 7-methylguanosine mRNA cap and facilitates translation.Proteomics · 2015Article
- New cell-signaling pathways for controlling cytomegalovirus replication.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2014Review
- Induction of stress granule-like structures in vesicular stomatitis virus-infected cells.Journal of virology · 2013Article
- Activation of the unfolded protein response by 2-deoxy-D-glucose inhibits Kaposi's sarcoma-associated herpesvirus replication and gene expression.Antimicrobial agents and chemotherapy · 2012Article
- Viral modulation of stress granules.Virus research · 2012Review
- Murine cytomegalovirus targets transcription factor ATF4 to exploit the unfolded-protein response.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We previously reported that human cytomegalovirus (HCMV) infection induces endoplasmic reticulum (ER) stress, resulting in activation of the unfolded protein response (UPR). Although some normal consequences of UPR activation (e.g., translation attenuation) are detrimental to viral infection, we have previously shown that HCMV infection adapts the UPR to benefit the viral infection (14). For example, UPR-induced translation attenuation is inhibited by viral infection, while potentially beneficial aspects of the UPR are maintained. In the present work, we tested the ability of HCMV to overcome a robust induction of the UPR by the drugs thapsigargin and clotrimazole (CLT), which disrupt ER calcium homeostasis. A 24-h treatment with these drugs beginning at 48, 72, or 96 h postinfection (hpi) completely inhibited further production of infectious virions. HCMV could not overcome the inhibition of global translation by CLT; however, between 48 and 72 hpi, HCMV overcame translational inhibition caused by thapsigargin. Despite the restoration of translation in thapsigargin, the accumulation of immediate-early and early gene products was modestly retarded (50% or less), whereas the accumulation of an early-late and late gene product was significantly retarded. Electron microscopic analysis shows that the drugs severely disrupt the maturation of HCMV virions. This can be accounted for by both the retarded accumulation of late gene products and the drug-induced depletion of ER calcium, which disrupts critical cellular functions needed for maturation.
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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.