ArticleNature microbiology2018
Human cytomegalovirus reprogrammes haematopoietic progenitor cells into immunosuppressive monocytes to achieve latency.
Article in Nature microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 95 citations in OpenAlex.
- The human cytomegalovirus vGPCR UL33 is essential for efficient lytic replication in epithelial cells.Journal of virology · 2026Article
- How stem cells respond to infection, inflammation and ageing.Nature reviews. Immunology · 2025Review
- The Immunoregulatory Mechanisms of Human Cytomegalovirus from Primary Infection to Reactivation.Pathogens (Basel, Switzerland) · 2025Review
- Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation.Journal of virology · 2025Article
- Cytomegalovirus latency-the sum of subtleties.Journal of virology · 2025Review
- Latent Human Cytomegalovirus Infection Activates the STING Pathway but p-IRF3 Translocation Is Limited.Viruses · 2025Article
- Why Are Cytomegalovirus-Encoded G-Protein-Coupled Receptors Essential for Infection but Only Variably Conserved?Pathogens (Basel, Switzerland) · 2025Review
- Human cytomegalovirus RNA2.7 inhibits ferroptosis by upregulating ferritin and GSH via promoting ZNF395 degradation.PLoS pathogens · 2024Article
- Cytomegalovirus Infections in Hematopoietic Stem Cell Transplant: Moving Beyond Molecular Diagnostics to Immunodiagnostics.Diagnostics (Basel, Switzerland) · 2024Review
- Delivery of US28 by incoming HCMV particles rapidly attenuates Akt activity to suppress HCMV lytic replication in monocytes.Science signaling · 2024Article
- STAT3-Mediated Ferroptosis is Involved in Sepsis-Associated Acute Respiratory Distress Syndrome.Inflammation · 2024Article
- Human cytomegalovirus and neonatal infection.Current research in microbial sciences · 2024Review
- Decoding human cytomegalovirus for the development of innovative diagnostics to detect congenital infection.Pediatric research · 2024Review
- Effect of Cytomegalovirus on the Immune System: Implications for Aging and Mental Health.Current topics in behavioral neurosciences · 2023Article
- Exogenous Interleukin-37 Alleviates Hepatitis with Reduced Dendritic Cells and Induced Regulatory T Cells in Acute Murine Cytomegalovirus Infection.Journal of immunology research · 2023Article
- Effect of B7-H4 downregulation induced by Toxoplasma gondii infection on dysfunction of decidual macrophages contributes to adverse pregnancy outcomes.Parasites & vectors · 2022Article
- Cytomegalovirus US28 regulates cellular EphA2 to maintain viral latency.Science advances · 2022Article
- First report of canine morbillivirus infection of adipose tissue-derived stem cells from dogs with distemper.Veterinary world · 2022Article
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11 authors at 6 institutions in 2 countries.
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Abstract
The precise cell type hosting latent human cytomegalovirus (HCMV) remains elusive. Here, we report that HCMV reprogrammes human haematopoietic progenitor cells (HPCs) into a unique monocyte subset to achieve latency. Unlike conventional monocytes, this monocyte subset possesses higher levels of B7-H4, IL-10 and inducible nitric oxide synthase (iNOS), a longer lifespan and strong immunosuppressive capacity. Cell sorting of peripheral blood from latently infected human donors confirms that only this monocyte subset, representing less than 0.1% of peripheral mononuclear cells, is HCMV genome-positive but immediate-early-negative. Mechanistic studies demonstrate that HCMV promotes the differentiation of HPCs into this monocyte subset by activating cellular signal transducer and activator of transcription 3 (STAT3). In turn, this monocyte subset generates a high level of nitric oxide (NO) to silence HCMV immediate-early transcription and promote viral latency. By contrast, the US28-knockout HCMV mutant, which is incapable of activating STAT3, fails to reprogramme the HPCs and achieve latency. Our findings reveal that via activating the STAT3-iNOS-NO axis, HCMV differentiates human HPCs into a longevous, immunosuppressive monocyte subset for viral latency.
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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.