ArticleFrontiers in cellular and infection microbiology2020
The Requirement for US28 During Cytomegalovirus Latency Is Independent of US27 and US29 Gene Expression.
Article in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 22 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
- Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation.Journal of virology · 2025Article
- Inhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34Antiviral research · 2025Article
- Why Are Cytomegalovirus-Encoded G-Protein-Coupled Receptors Essential for Infection but Only Variably Conserved?Pathogens (Basel, Switzerland) · 2025Review
- Third intracellular loop of HCMV US28 is necessary for signaling and viral reactivation.Journal of virology · 2025Article
- The Pentamer glycoprotein complex inhibits viral Immediate Early transcription during Human Cytomegalovirus infections.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Delivery of US28 by incoming HCMV particles rapidly attenuates Akt activity to suppress HCMV lytic replication in monocytes.Science signaling · 2024Article
- Cytomegalovirus US28 regulates cellular EphA2 to maintain viral latency.Science advances · 2022Article
- Article
- Review
- 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
- Understanding HCMV Latency Using Unbiased Proteomic Analyses.Pathogens (Basel, Switzerland) · 2020Review
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The ability to establish a latent infection with periodic reactivation events ensures herpesviruses, like human cytomegalovirus (HCMV), lifelong infection, and serial passage. The host-pathogen relationship throughout HCMV latency is complex, though both cellular and viral factors influence the equilibrium between latent and lytic infection. We and others have shown one of the viral-encoded G protein-coupled receptors, US28, is required for HCMV latency. US28 potentiates signals both constitutively and in response to ligand binding, and we previously showed deletion of the ligand binding domain or mutation of the G protein-coupling domain results in the failure to maintain latency similar to deletion of the entire US28 open reading frame (ORF). Interestingly, a recent publication detailed an altered phenotype from that previously reported, showing US28 is required for viral reactivation rather than latency, suggesting the US28 ORF deletion impacts transcription of the surrounding genes. Here, we show an independently generated US28-stop mutant, like the US28 ORF deletion mutant, fails to maintain latency in hematopoietic cells. Further, we found
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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.