ArticleJournal of virology2012
Human cytomegalovirus pUL78 G protein-coupled receptor homologue is required for timely cell entry in epithelial cells but not fibroblasts.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 59 citations in OpenAlex.
- The human cytomegalovirus vGPCR UL33 is essential for efficient lytic replication in epithelial cells.Journal of virology · 2026Article
- Human cytomegalovirus UL78 is a nuclear-localized GPCR necessary for efficient reactivation from latent infection in CD34Journal of virology · 2025Article
- The BTK-DDX41 axis of the STING pathway is activated during cytomegalovirus lytic infection.Journal of virology · 2025Article
- Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation.Journal of virology · 2025Article
- Why Are Cytomegalovirus-Encoded G-Protein-Coupled Receptors Essential for Infection but Only Variably Conserved?Pathogens (Basel, Switzerland) · 2025Review
- Article
- Review
- Deciphering the Potential Coding of Human Cytomegalovirus: New Predicted Transmembrane Proteome.International journal of molecular sciences · 2022Article
- Modulation of host cell signaling during cytomegalovirus latency and reactivation.Virology journal · 2021Review
- CMV-encoded GPCR pUL33 activates CREB and facilitates its recruitment to the MIE locus for efficient viral reactivation.Journal of cell science · 2021Article
- Methods for Studying the Function of Cytomegalovirus GPCRs.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Rat Cytomegalovirus Virion-Associated Proteins R131 and R129 Are Necessary for Infection of Macrophages and Dendritic Cells.Pathogens (Basel, Switzerland) · 2020Article
- Article
- Cytomegalovirus Latency and Reactivation: An Intricate Interplay With the Host Immune Response.Frontiers in cellular and infection microbiology · 2020Review
- Human Cytomegalovirus Primary Infection and Reactivation: Insights From Virion-Carried Molecules.Frontiers in microbiology · 2020Review
- The Requirement for US28 During Cytomegalovirus Latency Is Independent of US27 and US29 Gene Expression.Frontiers in cellular and infection microbiology · 2020Article
- Characterization of a live-attenuated HCMV-based vaccine platform.Scientific reports · 2019Article
- The human cytomegalovirus-encoded G protein-coupled receptor UL33 exhibits oncomodulatory properties.The Journal of biological chemistry · 2019Article
- Article
- Emerging roles of cytomegalovirus-encoded G protein-coupled receptors during lytic and latent infection.Medical microbiology and immunology · 2019Review
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
Human cytomegalovirus (HCMV) encodes four putative G protein-coupled receptors, including pUL78, whose rodent orthologues are known to be important for replication and spread in their hosts. To investigate the mechanism by which pUL78 contributes to viral replication and pathogenesis, we generated a derivative of the TB40/E clinical isolate of HCMV that is unable to express the receptor. Consistent with previous findings using laboratory strains of the virus, the mutant replicated normally in fibroblasts. Although laboratory strains are restricted to growth in fibroblasts, clinical isolates grow in many cell types, including epithelial and endothelial cells, in which the pUL78-deficient TB40/E derivative exhibited a growth defect. Infection with the mutant virus resulted in a significant decrease in viral RNA and protein expression. Although there was no difference in binding of the virus to the cell, we detected a delay in the entry and subsequent delivery of virion DNA and protein to the nuclei of epithelial cells following infection with the UL78 mutant virus. Taken together, our results demonstrate that pUL78 supports infection at a point after binding but before entry in epithelial cells, a cell type important for in vivo viral replication and spread.
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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.