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Updated: Jul 30, 2026

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
Temporal and spatial characterization of keratinocytes supporting orf virus replication
Byung-Joon Seung1, Sushil Khatiwada1, Daniel L Rock1
1Department of Pathobiology, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Orf virus (ORFV) replicates in specific differentiating skin cells, not proliferating ones, after wound-induced skin damage. This finding clarifies ORFV tropism and delayed replication in sheep and goats.
Area of Science:
- Veterinary Virology
- Dermatology
- Cell Biology
Background:
- Poxviruses typically infect keratinocytes, causing skin pathology.
- Orf virus (ORFV) causes localized skin infections in sheep and goats.
- ORFV replication is delayed and linked to epidermal damage and healing.
Purpose of the Study:
- To identify the specific keratinocyte subpopulation supporting ORFV replication.
- To elucidate the timing and cellular characteristics of ORFV replication during wound healing.
Main Methods:
- Utilized in situ hybridization, immunohistochemistry, and confocal microscopy.
- Employed quantitative PCR (qPCR) for viral detection.
- Developed a full-thickness wound/infection model in sheep.
Main Results:
- No viral transcription or DNA replication was detected during the initial 2-day eclipse phase.
- Viral transcription initiated between days 2 and 3 post-infection.
- Replication occurred in keratinocytes of the stratum granulosum and upper stratum spinosum, expressing differentiation markers (cytokeratin 10, 6, filaggrin, loricrin) and negative for proliferation marker Ki-67.
Conclusions:
- ORFV replication is restricted to keratinocytes undergoing advanced differentiation, not proliferation.
- This cellular tropism explains the delayed replication observed during wound healing.
- Findings provide insights into ORFV pathogenesis and host-cell interactions.
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