ArticleJournal of periodontal research2025
Herpesvirus Simplex Virus-1 Exploits Inflammation to Infect Periodontal Stem Cells and Disrupt Lineage Commitment.
Article in Journal of periodontal research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Longitudinal Salivary Immunophenotyping Reveals Distinct Cellular Signatures of Periodontal Disease Activity and Resolution.bioRxiv : the preprint server for biology · 2026Article
- Herpesvirus Simplex Virus-1 Exploits Inflammation to Infect Periodontal Stem Cells and Disrupt Lineage Commitment.Journal of periodontal research · 2025Article
- A Protocol for Modeling Human Bone Inflammation: Co-Culture of Osteoblasts and Osteoclasts Exposed to Different Inflammatory Microenvironments.Methods and protocols · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
aimsElevated levels of Herpes Simplex Virus 1 (HSV-1) have been reported in periodontitis, however, the tropism and relationship with periodontal inflammation are poorly characterized. This study investigated how inflammation affects viral tropism toward human periodontal ligament stem cells (hPDLSCs).
methodsHSV-1 gB and gD transcripts in healthy and diseased human gingiva were measured by RT-qPCR and confirmed in HSV-1-infected murine gingiva. HSV-1 infection in hPDLSCs was analyzed by imaging and flow cytometry. hPDLSCs were individually treated with IL-6, TNF-α, GMCSF, IL-10, or PgLPS, and HSV-1 replication was assessed by infecting with the 17 GFP strain. Lineage markers in virally infected hPDLSCs during osteogenic differentiation were measured by RT-qPCR and immunofluorescence in vitro and validated in vivo. Mice subjected to ligature-induced periodontitis (LIP) and infected with HSV-1 were examined for gingival histology, inflammatory cytokines, and alveolar bone loss.
resultsInflamed human gingiva showed higher expression of viral transcripts compared to healthy controls. In mouse oral HSV-1 infection, gB and gD expression increased over time, with higher levels in mice with ligature-induced periodontitis. Virus infected hPDLSCs challenged with inflammatory mediators or PgLPS showed higher GFP, while IL-10 treatment attenuated GFP levels. Importantly, HSV-1 17 GFP infection affected osteoblast lineage commitment by promoting the expression of key transcription factors in vitro and in vivo. Compared to the LIP alone group, higher levels of inflammatory markers and bone loss were evident in HSV-1 infected with LIP.
conclusionhPDLSCs are trophic to HSV-1 in vitro and in vivo, with periodontal inflammation playing a significant role in viral tropism.
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What Socratic 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 Socratic graph.