ArticleJournal of virology2014
Interactions between herpesvirus entry mediator (TNFRSF14) and latency-associated transcript during herpes simplex virus 1 latency.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 46 citations in OpenAlex.
- HSV-1 LAT promotes ocular diseases in the absence of type I IFN responses in sensory neurons.Journal of virology · 2026Article
- Complete disruption of gD binding to HVEM alters virus replication and host receptor homeostasis.PLoS pathogens · 2026Article
- Partial or complete blocking of gD binding to HVEM affects primary and latent HSV-1 infection as well as eye disease in HSV-1 infected mice.PLoS pathogens · 2026Article
- Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.Investigative ophthalmology & visual science · 2026Article
- In the Absence of Type-1 IFN, HSV-1 LAT Increases γ34.5 Expression and Enhances Mortality in Infected Mice.Viruses · 2025Article
- IFNβ absence compensates for LAT functions in latency reactivation and T cell exhaustion.Journal of virology · 2025Article
- The importance of IFNα2A (Roferon-A) in HSV-1 latency and T cell exhaustion in ocularly infected mice.PLoS pathogens · 2024Article
- A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript.Viruses · 2024Review
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
- The anti-apoptotic function of HSV-1 LAT in neuronal cell cultures but not its function during reactivation correlates with expression of two small non-coding RNAs, sncRNA1&2.PLoS pathogens · 2024Article
- Binding of herpesvirus entry mediator (HVEM) and HSV-1 gD affect reactivation but not latency levels.PLoS pathogens · 2023Article
- Stacking the odds: Multiple sites for HSV-1 latency.Science advances · 2023Article
- Impact of actin polymerization and filopodia formation on herpes simplex virus entry in epithelial, neuronal, and T lymphocyte cells.Frontiers in cellular and infection microbiology · 2023Review
- Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice.PLoS pathogens · 2022Article
- The Role of Latency-Associated Transcripts in the Latent Infection of Pseudorabies Virus.Viruses · 2022Review
- Small Noncoding RNA (sncRNA1) within the Latency-Associated Transcript Modulates Herpes Simplex Virus 1 Virulence and the Host Immune Response during Acute but Not Latent Infection.Journal of virology · 2022Article
- Herpes Simplex Virus 1 Small Noncoding RNAs 1 and 2 Activate the Herpesvirus Entry Mediator Promoter.Journal of virology · 2022Article
- Essential role of M1 macrophages in blocking cytokine storm and pathology associated with murine HSV-1 infection.PLoS pathogens · 2021Article
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- Blocking HSV-1 glycoprotein K binding to signal peptide peptidase reduces virus infectivity in vitro and in vivo.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Herpesvirus entry mediator (HVEM) is one of several cell surface proteins herpes simplex virus (HSV) uses for attachment/entry. HVEM regulates cellular immune responses and can also increase cell survival. Interestingly, latency-associated transcript (LAT), the only viral gene consistently expressed during neuronal latency, enhances latency and reactivation by promoting cell survival and by helping the virus evade the host immune response. However, the mechanisms of these LAT activities are not well understood. We show here for the first time that one mechanism by which LAT enhances latency and reactivation appears to be by upregulating HVEM expression. HSV-1 latency/reactivation was significantly reduced in Hvem(-/-) mice, indicating that HVEM plays a significant role in HSV-1 latency/reactivation. Furthermore, LAT upregulated HVEM expression during latency in vivo and also when expressed in vitro in the absence of other viral factors. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially through binding of two LAT small noncoding RNAs to the HVEM promoter and that the increased HVEM then leads to downregulation of immune responses in the latent microenvironment and increased survival of latently infected cells. Thus, one of the mechanisms by which LAT enhances latency/reactivation appears to be through increasing expression of HVEM.
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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.