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Herpesvirus Simplex Virus-1 Exploits Inflammation to Infect Periodontal Stem Cells and Disrupt Lineage Commitment.

Araceli Valverde1, Raza Ali Naqvi1, Yinghua Chen2

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Periodontal inflammation enhances Herpes Simplex Virus 1 (HSV-1) tropism toward human periodontal ligament stem cells (hPDLSCs). HSV-1 infection also impairs osteoblast differentiation and exacerbates bone loss in periodontitis.

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Area of Science:

  • Oral biology
  • Virology
  • Stem cell biology

Background:

  • Herpes Simplex Virus 1 (HSV-1) is linked to periodontitis, but its specific tropism and relationship with periodontal inflammation are unclear.
  • Human periodontal ligament stem cells (hPDLSCs) are crucial for periodontal tissue regeneration.

Purpose of the Study:

  • To investigate how periodontal inflammation influences HSV-1 tropism towards hPDLSCs.
  • To determine the impact of HSV-1 infection on hPDLSC osteogenic differentiation and its role in periodontitis-associated bone loss.

Main Methods:

  • Quantified HSV-1 transcripts (gB, gD) in human and murine gingiva using RT-qPCR.
  • Analyzed HSV-1 infection in hPDLSCs via imaging and flow cytometry, assessing replication after exposure to inflammatory mediators (IL-6, TNF-α, GMCSF, IL-10, PgLPS).
  • Evaluated osteogenic differentiation markers in HSV-1 infected hPDLSCs in vitro and in vivo, alongside histological and cytokine analysis in a ligature-induced periodontitis (LIP) mouse model.

Main Results:

  • Inflamed gingiva exhibited higher HSV-1 transcript levels compared to healthy controls.
  • HSV-1 replication in hPDLSCs increased with inflammatory mediators (except IL-10) and PgLPS.
  • HSV-1 infection inhibited osteoblast lineage commitment in hPDLSCs, promoting key transcription factors.
  • HSV-1 infected mice with LIP showed exacerbated inflammatory markers and alveolar bone loss.

Conclusions:

  • hPDLSCs are susceptible to HSV-1 infection both in vitro and in vivo.
  • Periodontal inflammation significantly enhances HSV-1 tropism to hPDLSCs.
  • HSV-1 infection negatively impacts hPDLSC osteogenic potential and worsens periodontitis progression.