ArticleProceedings of the National Academy of Sciences of the United States of America2003
Human cytomegalovirus UL83-coded pp65 virion protein inhibits antiviral gene expression in infected cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
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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
130 citing papers in PubMed, 197 citations in OpenAlex.
- Nuclear transport of human cytomegalovirus tegument protein pp65 through nucleoplasmic reticulum.PLoS pathogens · 2026Article
- Breaking barriers: how cytomegaloviruses manipulate myeloid cells to invade tissues.EMBO reports · 2026Review
- NK and T cell evasion mechanism of human cytomegalovirus.Archives of virology · 2025Review
- The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.Journal of virology · 2025Article
- Applications of CRISPR-Cas-Based Genome Editing Approaches Against Human Cytomegalovirus Infection.Biomedicines · 2025Review
- Protein-S-nitrosylation of human cytomegalovirus pp65 reduces its ability to undermine cGAS.Journal of virology · 2025Article
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- The battle between the innate immune cGAS-STING signaling pathway and human herpesvirus infection.Frontiers in immunology · 2023Review
- Effect of Cytomegalovirus on the Immune System: Implications for Aging and Mental Health.Current topics in behavioral neurosciences · 2023Article
- Temporal dynamics of HCMV gene expression in lytic and latent infections.Cell reports · 2022Article
- Viral dUTPases: Modulators of Innate Immunity.Biomolecules · 2022Review
- Human Cytomegalovirus miR-US33as-5p Targets IFNAR1 to Achieve Immune Evasion During Both Lytic and Latent Infection.Frontiers in immunology · 2021Article
- Human Cytomegalovirus UL23 Attenuates Signal Transducer and Activator of Transcription 1 Phosphorylation and Type I Interferon Response.Frontiers in microbiology · 2021Article
- Protein S-Nitrosylation of Human Cytomegalovirus pp71 Inhibits Its Ability To Limit STING Antiviral Responses.Journal of virology · 2020Article
- Cytomegaloviruses and Macrophages-Friends and Foes From Early on?Frontiers in immunology · 2020Review
- Tuning the Orchestra: HCMV vs. Innate Immunity.Frontiers in microbiology · 2020Review
- Computational assembly of a human Cytomegalovirus vaccine upon experimental epitope legacy.BMC bioinformatics · 2019Article
- UJournal of virology · 2019Article
- HCMV-encoded US7 and US8 act as antagonists of innate immunity by distinctively targeting TLR-signaling pathways.Nature communications · 2019Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The initial interaction of human cytomegalovirus with fibroblasts triggers, and then partially blocks, an innate immune response pathway that leads to the induction of IFN-responsive genes and proinflammatory chemokines. Infection of fibroblasts with human cytomegalovirus inhibited their ability to respond to exogenous IFN. Consistent with the observation that the block did not depend on de novo viral protein synthesis, ectopic expression of the viral UL83-coded pp65, an abundant virion protein, inhibited IFN signaling. Furthermore, DNA array analysis showed that infection with a pp65-deficient mutant virus caused a much stronger induction of many IFN-response and proinflammatory chemokine RNAs than infection with wild-type virus. The nuclear DNA-binding activities of transcription factors NF-kappaB and IRF1 were induced to a much greater extent after infection with the pp65-deficient mutant than with wild-type virus. IFN-stimulated gene factor 3 DNA-binding was modestly enhanced, whereas IRF3 activity was not affected by mutation of pp65. Together, these results imply that pp65, which is delivered to newly infected cells in the virion, antagonizes a pathway that affects NF-kappaB and IRF1 and prevents the accumulation of mRNAs encoded by numerous cellular antiviral genes.
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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.