ArticleJournal of virology2018
Extracellular Vesicles Released by Herpes Simplex Virus 1-Infected Cells Block Virus Replication in Recipient Cells in a STING-Dependent Manner.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 86 citations in OpenAlex.
- Oncolytic Virus-Engineered Extracellular Vesicles Rewire Glioblastoma Immunity.Journal of extracellular vesicles · 2026Article
- Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.bioRxiv : the preprint server for biology · 2026Article
- When Viruses Talk through Extracellular Vesicles: a New Perspective on Sars-Cov-2-Induced Neurodegeneration.Journal of extracellular vesicles · 2026Article
- Nuclear translocation of Sp100A suppresses multiple DNA viruses and limits HSV-1 lytic replication in vivo.Virologica Sinica · 2026Article
- Intercellular highways of viral spread: tunneling nanotubes and extracellular vesicles at the maternal-fetal interface.Current opinion in virology · 2025Review
- Review
- Neurodegeneration as Ecosystem Failure: A New Paradigm for Prevention and Treatment.International journal of molecular sciences · 2025Review
- Article
- Extracellular vesicles: Antiviral functions and applications in therapeutics and vaccines.iScience · 2025Review
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Extracellular Vesicles Released by Bovine Alphaherpesvirus 1-Infected A549 Cells May Limit Subsequent Infections of the Progeny Virus.International journal of molecular sciences · 2025Article
- Review
- HSV-1 virions and related particles: biogenesis and implications in the infection.Journal of virology · 2025Review
- Dual Role of Extracellular Vesicles as Orchestrators of Emerging and Reemerging Virus Infections.Cell biochemistry and biophysics · 2025Review
- Recruitment of apolipoprotein E facilitates Herpes simplex virus 1 attachment and release.Npj viruses · 2025Article
- Extracellular vesicles promote the infection and pathogenicity of Japanese encephalitis virus.Journal of extracellular vesicles · 2025Article
- Neutral sphingomyelinase 2: A promising drug target for CNS disease.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Keratinocyte derived extracellular vesicles mediated crosstalk between epidermis and dermis in UVB-induced skin inflammation.Cell communication and signaling : CCS · 2024Article
- Article
- Exploring the role of brain-derived extracellular vesicles in viral infections: from pathological insights to biomarker potential.Frontiers in cellular and infection microbiology · 2024Review
8 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
Herpes simplex virus 1 (HSV-1)-infected cells release extracellular vesicles (EVs) that deliver to uninfected cells viral factors and host components, such as the stimulator of interferon genes (STING), which activates type I interferon upon foreign DNA sensing. The functions of EVs released by HSV-1-infected cells have remained unknown. Here, we describe a procedure to separate the EVs from HSV-1 virions that is based on an iodixanol/sucrose gradient. STING, along with the EV markers CD63 and CD9, was found in light-density fractions, while HSV components accumulated in heavy-density fractions. HSV-1 infection stimulated the release of EVs from the cells. The EVs derived from infected cells, but not from uninfected cells, activated innate immunity in recipient cells and suppressed viral gene expression and virus replication. Moreover, only the EVs derived from infected cells stimulated the expression of a subset of M1-type markers in recipient macrophages. Conversely, EVs derived from STING-knockdown cells failed to stimulate the expression of these M1-type markers, they activated innate immune responses to a lesser extent in recipient cells, and they did not sustain the inhibition of virus replication. These data suggest that STING from the EV donor cells contributes to the antiviral responses in cells receiving EVs from HSV-1-infected cells. Perturbations in the biogenesis of EVs by silencing CD63 or blocking the activity of the neutral spingomyelinase-2 (nSMase-2) increased the HSV-1 yields. Overall, our data suggest that the EVs released from HSV-1-infected cells negatively impact the infection and could control the dissemination of the virus.
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What OpenQuestion holds
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.