ArticlemBio2021
Human Cytomegalovirus Uses a Host Stress Response To Balance the Elongation of Saturated/Monounsaturated and Polyunsaturated Very-Long-Chain Fatty Acids.
Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Glutamine supports human cytomegalovirus induced lipidome remodeling through reductive carboxylation.PLoS pathogens · 2026Article
- Intratumoral microbiota in cancer: molecular mechanism and therapeutic strategies.Molecular biomedicine · 2026Review
- Metabolomics Highlights Reduced Glutamate and Acetylcarnitine in the Amniotic Fluid of Cytomegalovirus-Infected Pregnant Women.Journal of proteome research · 2026Article
- Metabolic hijackers: how viral proteins redefine host cell landscapes.Journal of virology · 2026Review
- Glutamine supports human cytomegalovirus induced lipidome remodeling through reductive carboxylation.bioRxiv : the preprint server for biology · 2026Article
- Human cytomegalovirus promotesJournal of virology · 2025Article
- The p97 ATPase and its adaptor UBXD8 maintain peroxisome pools by preventing pexophagy.The Journal of cell biology · 2025Article
- PINLYP-mediated phospholipid metabolism reprogramming contributes to chronic herpesvirus infection.PLoS pathogens · 2025Article
- Human cytomegalovirus promotesbioRxiv : the preprint server for biology · 2025Article
- HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis.Journal of virology · 2025Article
- Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cytomegalovirus drives Vδ1Nature communications · 2024Article
- Liver X Receptor-Inducible Host E3 Ligase IDOL Targets a Human Cytomegalovirus Reactivation Determinant.Journal of virology · 2023Article
- Acute murine cytomegalovirus infection boosts cell-type specific response and lipid metabolism changes in the liver of infant mice.Frontiers in immunology · 2023Article
- Cholesterol Biosynthesis Modulates CSFV Replication.Viruses · 2022Article
- Article
- Shear-Mediated Platelet Activation is Accompanied by Unique Alterations in Platelet Release of Lipids.Cellular and molecular bioengineering · 2021Article
- Viral Infection Drives the Regulation of Feeding Behavior Related Genes inInternational journal of molecular sciences · 2021Article
- Oncolytic Virus-Induced Autophagy in Glioblastoma.Cancers · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress and virus infection regulate lipid metabolism. Human cytomegalovirus (HCMV) infection induces fatty acid (FA) elongation and increases the abundance of lipids with very-long-chain FA (VLCFA) tails. While reprogramming of metabolism can be stress related, the role of stress in HCMV reprogramming of lipid metabolism is poorly understood. In this study, we engineered cells to knock out protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) in the ER stress pathway and measured lipid changes using lipidomics to determine if PERK is needed for lipid changes associated with HCMV infection. In HCMV-infected cells, PERK promotes increases in the levels of phospholipids with saturated FA (SFA) and monounsaturated FA (MUFA) VLCFA tails. Further, PERK enhances FA elongase 7 (ELOVL7) protein levels, which elongates SFA and MUFA VLCFAs. Additionally, we found that increases in the elongation of polyunsaturated fatty acids (PUFAs) associated with HCMV infection were independent of PERK and that lipids with PUFA tails accumulated in HCMV-infected PERK knockout cells. Additionally, the protein levels of ELOVL5, which elongates PUFAs, are increased by HCMV infection through a PERK-independent mechanism. These observations show that PERK differentially regulates ELOVL7 and ELOVL5, creating a balance between the synthesis of lipids with SFA/MUFA tails and PUFA tails. Additionally, we found that PERK was necessary for virus replication and the infectivity of released viral progeny. Overall, our findings indicate that PERK-and, more broadly, ER stress-may be necessary for the membrane biogenesis needed to generate infectious HCMV virions.
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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 Socratic graph.