ArticleJournal of virology2007
Human cytomegalovirus UL38 protein blocks apoptosis.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 164 citations in OpenAlex.
- Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026Review
- HCMV-pUS2 Disrupts cGAS-STING Signaling through LMAN2L Degradation.PLoS pathogens · 2026Article
- Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cytotoxic lymphocytes counteract viral type I interferon immune evasion.PLoS pathogens · 2026Article
- Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Human cytomegalovirus promotesJournal of virology · 2025Article
- RNA-targeted proteomics identifies YBX1 as critical for efficient HCMV mRNA translation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Human cytomegalovirus promotesbioRxiv : the preprint server for biology · 2025Article
- Review
- Human cytomegalovirus infection induces L1 expression through UL38-dependent mTOR-KAP1 pathway.PloS one · 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
- Structure-based design of a soluble human cytomegalovirus glycoprotein B antigen stabilized in a prefusion-like conformation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- No Time to Die: How Cytomegaloviruses Suppress Apoptosis, Necroptosis, and Pyroptosis.Viruses · 2024Review
- Pseudorabies virus UL38 attenuates the cGAS-STING signaling pathway by recruiting Tollip to promote STING for autophagy degradation.Virology journal · 2024Article
- Article
- CCR4-NOT differentially controls host versus virus poly(a)-tail length and regulates HCMV infection.EMBO reports · 2023Article
- ADAM17 targeting by human cytomegalovirus remodels the cell surface proteome to simultaneously regulate multiple immune pathways.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Human cytomegalovirus attenuates AKT activity by destabilizing insulin receptor substrate proteins.bioRxiv : the preprint server for biology · 2023Article
- Differential effects of CMV infection on the viability of cardiac cells.Cell death discovery · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Apoptosis is an innate cellular defense response to viral infection. The slow-replicating human cytomegalovirus (HCMV) blocks premature death of host cells prior to completion of the infection cycle. In this study, we report that the HCMV UL38 gene encodes a cell death inhibitory protein. A mutant virus lacking the pUL38 coding sequence, ADdlUL38, grew poorly in human fibroblasts, failed to accumulate viral DNA to wild-type levels, and induced excessive death of infected cells. Cells expressing pUL38 were resistant to cell death upon infection and effectively supported the growth of ADdlUL38. Cells infected with the pUL38-deficient virus showed morphological changes characteristic of apoptosis, including cell shrinkage, membrane blebbing, vesicle release, and chromatin condensation and fragmentation. The proteolytic cleavage of two key enzymes involved in apoptosis, namely, caspase 3 and poly(ADP-ribose) polymerase, was activated upon ADdlUL38 infection, and the cleavage was blocked in cells expressing pUL38. The pan-caspase inhibitor Z-VAD-FMK largely restored the growth of ADdlUL38 in normal fibroblasts, indicating that the defective growth of the mutant virus mainly resulted from premature death of host cells. Furthermore, cells expressing pUL38 were resistant to cell death induced by a mutant adenovirus lacking the antiapoptotic E1B-19K protein or by thapsigargin, which disrupts calcium homeostasis in the endoplasmic reticulum. Taken together, these results indicate that the HCMV protein pUL38 suppresses apoptosis, blocking premature death of host cells to facilitate efficient virus 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.