ArticleJournal of virology2008
Lymphoid-related CD11c+ CD8alpha+ dendritic cells are involved in enhancing herpes simplex virus type 1 latency.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 40 citations in OpenAlex.
- Herpes simplex virus type 1 interferes with signal transducer and activator of transcription 3 expression in infected mature dendritic cells.The Journal of general virology · 2026Article
- 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
- Stacking the odds: Multiple sites for HSV-1 latency.Science advances · 2023Article
- 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
- Suppression of CD80 Expression by ICP22 Affects Herpes Simplex Virus Type 1 Replication and CD8Journal of virology · 2021Article
- Pathobiology and treatment of viral keratitis.Experimental eye research · 2021Review
- 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
- CD80 Plays a Critical Role in Increased Inflammatory Responses in Herpes Simplex Virus 1-Infected Mouse Corneas.Journal of virology · 2020Article
- Loss of ICP22 in HSV-1 Elicits Immune Infiltration and Maintains Stromal Keratitis Despite Reduced Primary and Latent Virus Infectivity.Investigative ophthalmology & visual science · 2019Article
- Herpes Simplex Virus 1 ICP22 Suppresses CD80 Expression by Murine Dendritic Cells.Journal of virology · 2019Article
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- CCR2+ migratory macrophages with M1 status are the early-responders in the cornea of HSV-1 infected mice.PloS one · 2019Article
- The Chemokine Receptor CXCR4 Mediates Recruitment of CD11c+ Conventional Dendritic Cells Into the Inflamed Murine Cornea.Investigative ophthalmology & visual science · 2018Article
- An M2 Rather than a TJournal of virology · 2018Article
- Effective Priming of Herpes Simplex Virus-Specific CD8Journal of virology · 2018Article
- Roles of M1 and M2 Macrophages in Herpes Simplex Virus 1 Infectivity.Journal of virology · 2017Article
- Interrelationship of Primary Virus Replication, Level of Latency, and Time to Reactivation in the Trigeminal Ganglia of Latently Infected Mice.Journal of virology · 2016Article
- CD8+ T Cells Play a Bystander Role in Mice Latently Infected with Herpes Simplex Virus 1.Journal of virology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism(s) by which herpes simplex virus type 1 (HSV-1) latency is established in neurons is not known. In this study, we examined the effect of dendritic cells (DCs) on the level of HSV-1 latency in trigeminal ganglia (TGs) of ocularly infected BALB/c and C57BL/6 mice. We found that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which increases the number of DCs, increased the amount of latency in infected mice. Conversely, depletion of DCs was associated with reduced latency. Latency was also significantly reduced in Flt3L(-/-) and CD8(-/-) mice. Interestingly, immunization of Flt3L(-/-) but not CD8(-/-) mice with Flt3L DNA increased latency. Transfer experiments using DCs expanded ex vivo with Flt3L or granulocyte-macrophage colony-stimulating factor suggested that increased latency was associated with the presence of lymphoid-related (CD11c(+) CD8alpha(+)) DCs, while reduced latency was associated with myeloid-related (CD11c(+) CD8alpha(-)) DCs. Modulation of DC numbers by Flt3L DNA immunization or depletion did not alter acute virus replication in the eye or TG or eye disease in ocularly infected mice. Our results suggest that CD11c(+) CD8alpha(+) DCs directly or indirectly increase the amount of HSV-1 latency in mouse TGs.
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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.