ArticleClinical and vaccine immunology : CVI2008
Role of dendritic cells in enhancement of herpes simplex virus type 1 latency and reactivation in vaccinated mice.
Article in Clinical and vaccine immunology : CVI, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 48 citations in OpenAlex.
- IFNβ absence compensates for LAT functions in latency reactivation and T cell exhaustion.Journal of virology · 2025Article
- A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript.Viruses · 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
- Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice.PLoS pathogens · 2022Article
- Review
- 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
- Essential role of M1 macrophages in blocking cytokine storm and pathology associated with murine HSV-1 infection.PLoS pathogens · 2021Article
- Suppression of CD80 Expression by ICP22 Affects Herpes Simplex Virus Type 1 Replication and CD8Journal of virology · 2021Article
- Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection.Frontiers in immunology · 2021Review
- Restoring Herpesvirus Entry Mediator (HVEM) Immune Function in HVEMJournal of virology · 2020Article
- Role of TH17 Responses in Increasing Herpetic Keratitis in the Eyes of Mice Infected with HSV-1.Investigative ophthalmology & visual science · 2020Article
- Expression of Murine CD80 by Herpes Simplex Virus 1 in Place of Latency-Associated Transcript (LAT) Can Compensate for Latency Reactivation and Anti-apoptotic Functions of LAT.Journal of virology · 2020Article
- CD80 Plays a Critical Role in Increased Inflammatory Responses in Herpes Simplex Virus 1-Infected Mouse Corneas.Journal of virology · 2020Article
- Roles of Type 1, 2, and 3 Innate Lymphoid Cells in Herpes Simplex Virus 1 InfectionJournal of virology · 2019Article
- CCR2+ migratory macrophages with M1 status are the early-responders in the cornea of HSV-1 infected mice.PloS one · 2019Article
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- Article
- The Chemokine Receptor CXCR4 Mediates Recruitment of CD11c+ Conventional Dendritic Cells Into the Inflamed Murine Cornea.Investigative ophthalmology & visual science · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ocular infection with herpes simplex virus type 1 (HSV-1) frequently leads to recurrent infection, which is a major cause of corneal scarring. Thus, the prevention of the establishment of latency should be a primary goal of vaccination against HSV-1. To this end, we have examined the contribution of dendritic cells (DCs) to the efficacy of a vaccine against ocular HSV-1 infection. Transgenic mice (expressing a CD11c-diphtheria toxin receptor-green fluorescent protein construct) with a BALB/c background were immunized with a vaccine consisting of DNA that encodes five HSV-1 glycoproteins or were immunized with vector control DNA. The vaccinated mice were then depleted of their DCs through the injection of diphtheria toxin before and after ocular challenge with HSV-1. Analyses of HSV-1 replication in the eye, blepharitis, corneal scarring, and the survival of the infected mice upon primary infection indicated that DC depletion neither promoted nor compromised the efficacy of the vaccine. In contrast, DC depletion was associated with an approximately fivefold reduction in the level of latent virus in the trigeminal ganglia (TGs) of latently infected mice, as well as a significant reduction in the reactivation rate of latent virus. The possibility that DCs enhance the latency of HSV-1 in the TGs of ocularly infected mice suggests for the first time that DCs, rather than acting as "immune saviors," can exacerbate disease and compromise vaccine efficacy by enhancing viral latency and reactivation.
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