ArticleNature communications2017
Targeting the latent cytomegalovirus reservoir with an antiviral fusion toxin protein.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
48 citing papers in PubMed, 80 citations in OpenAlex.
- Targeting of Kaposi's sarcoma-associated herpesvirus by immunotoxins directed against the viral G protein-coupled receptor, ORF74.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation.Journal of virology · 2025Article
- Distinct Immunological Landscapes of HCMV-Specific T Cells in Bone Marrow and Peripheral Blood.Pathogens (Basel, Switzerland) · 2025Article
- The human cytomegalovirus-encoded pUS28 antagonizes CD4+ T cell recognition by targeting CIITA.eLife · 2025Article
- Why Are Cytomegalovirus-Encoded G-Protein-Coupled Receptors Essential for Infection but Only Variably Conserved?Pathogens (Basel, Switzerland) · 2025Review
- CMV Retinitis in the Context of SARS-CoV-2 Infection: A Case Study and Comprehensive Review of Viral Interactions.Pathogens (Basel, Switzerland) · 2024Review
- Virus-Specific Nanobody-Chimeras Degrade the Human Cytomegalovirus US28 Protein in CD34+ Cells.Pathogens (Basel, Switzerland) · 2024Article
- Delivery of US28 by incoming HCMV particles rapidly attenuates Akt activity to suppress HCMV lytic replication in monocytes.Science signaling · 2024Article
- Therapeutic targeting of HCMV-encoded chemokine receptor US28: Progress and challenges.Frontiers in immunology · 2023Review
- Cytomegalovirus US28 regulates cellular EphA2 to maintain viral latency.Science advances · 2022Article
- Viral G Protein-Coupled Receptors Encoded by β- and γ-Herpesviruses.Annual review of virology · 2022Review
- The Human Cytomegalovirus β2.7 Long Non-Coding RNA Prevents Induction of Reactive Oxygen Species to Maintain Viral Gene Silencing during Latency.International journal of molecular sciences · 2022Article
- A Viral Long Non-Coding RNA Protects against Cell Death during Human Cytomegalovirus Infection of CD14+ Monocytes.Viruses · 2022Article
- Epstein-Barr Virus-Encoded BILF1 Orthologues From Porcine Lymphotropic Herpesviruses Display Common Molecular Functionality.Frontiers in endocrinology · 2022Article
- Modulation of host cell signaling during cytomegalovirus latency and reactivation.Virology journal · 2021Review
- Cytomegalovirus Infections in Children with Primary and Secondary Immune Deficiencies.Viruses · 2021Review
- Review
- Review
- Virus-specific memory T cell responses unmasked by immune checkpoint blockade cause hepatitis.Nature communications · 2021Article
- Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Reactivation of human cytomegalovirus (HCMV) in transplant recipients can cause life-threatening disease. Consequently, for transplant recipients, killing latently infected cells could have far-reaching clinical benefits. In vivo, myeloid cells and their progenitors are an important site of HCMV latency, and one viral gene expressed by latently infected myeloid cells is US28. This viral gene encodes a cell surface G protein-coupled receptor (GPCR) that binds chemokines, triggering its endocytosis. We show that the expression of US28 on the surface of latently infected cells allows monocytes and their progenitor CD34+ cells to be targeted and killed by F49A-FTP, a highly specific fusion toxin protein that binds this viral GPCR. As expected, this specific targeting of latently infected cells by F49A-FTP also robustly reduces virus reactivation in vitro. Consequently, such specific fusion toxin proteins could form the basis of a therapeutic strategy for eliminating latently infected cells before haematopoietic stem cell transplantation.
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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.