ArticleJournal of virology2003
Human cytomegalovirus infection inhibits tumor necrosis factor alpha (TNF-alpha) signaling by targeting the 55-kilodalton TNF-alpha receptor.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
- Cytomegalovirus Infection Affects the Differentiation and Determines the Functionality of a Human Progenitor Neural Cell Line.Current microbiology · 2025Article
- Viral MicroRNAs in Herpes Simplex Virus 1 Pathobiology.Current pharmaceutical design · 2024Review
- 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
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.Molecular biology · 2022Article
- Cytomegalovirus Hepatitis in Immunocompetent and Immunocompromised Hosts.Journal of clinical and translational hepatology · 2021Review
- Molecular mechanisms of human herpes viruses inferring with host immune surveillance.Journal for immunotherapy of cancer · 2020Review
- Human Cytomegalovirus Decreases Major Histocompatibility Complex Class II by Regulating Class II Transactivator Transcript Levels in a Myeloid Cell Line.Journal of virology · 2020Article
- Novel Strategies to Combat CMV-Related Cardiovascular Disease.Pathogens & immunity · 2020Review
- HCMV-encoded US7 and US8 act as antagonists of innate immunity by distinctively targeting TLR-signaling pathways.Nature communications · 2019Article
- Human cytomegalovirus induces and exploits Roquin to counteract the IRF1-mediated antiviral state.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Hepatitis C Virus Exploits Death Receptor 6-mediated Signaling Pathway to Facilitate Viral Propagation.Scientific reports · 2017Article
- Cooperative inhibition of RIP1-mediated NF-κB signaling by cytomegalovirus-encoded deubiquitinase and inactive homolog of cellular ribonucleotide reductase large subunit.PLoS pathogens · 2017Article
- Article
- Utilizing a TLR5-Adjuvanted Cytomegalovirus as a Lentiviral Vaccine in the Nonhuman Primate Model for AIDS.PloS one · 2016Article
- Suppression of RIP3-dependent necroptosis by human cytomegalovirus.The Journal of biological chemistry · 2015Article
- The human cytomegalovirus UL26 protein antagonizes NF-κB activation.Journal of virology · 2014Article
- Human cytomegalovirus suppresses Fas expression and function.The Journal of general virology · 2014Article
- Cytomegalovirus miRNAs target secretory pathway genes to facilitate formation of the virion assembly compartment and reduce cytokine secretion.Cell host & microbe · 2014Article
- The intimate relationship between human cytomegalovirus and the dendritic cell lineage.Frontiers in microbiology · 2014Review
- Latency-associated degradation of the MRP1 drug transporter during latent human cytomegalovirus infection.Science (New York, N.Y.) · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Infection with human cytomegalovirus (HCMV) results in complex interactions between viral and cellular factors which perturb many cellular functions. HCMV is known to target the cell cycle, cellular transcription, and immunoregulation, and it is believed that this optimizes the cellular environment for viral DNA replication during productive infection or during carriage in the latently infected host. Here, we show that HCMV infection also prevents external signaling to the cell by disrupting the function of TNFRI, the 55-kDa receptor for tumor necrosis factor alpha (TNF-alpha), one of the receptors for a potent cytokine involved in eliciting a wide spectrum of cellular responses, including antiviral responses. HCMV infection of fully permissive differentiated monocytic cell lines and U373 cells resulted in a reduction in cell surface expression of TNFRI. The reduction appeared to be due to relocalization of TNFRI from the cell surface and was reflected in the elimination of TNF-alpha-induced Jun kinase activity. Analysis of specific phases of infection suggested that viral early gene products were responsible for this relocalization. However, a mutant HCMV in which all viral gene products known to be involved in down-regulation of major histocompatibility complex (MHC) class I were deleted still resulted in relocalization of TNFRI. Consequently, TNFRI relocalization by HCMV appears to be mediated by a novel viral early function not involved in down-regulation of cell surface MHC class I expression. We suggest that upon infection, HCMV isolates the cell from host-mediated signals, forcing the cell to respond only to virus-specific signals which optimize the cell for virus production and effect proviral responses from bystander cells.
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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.