ArticlePLoS pathogens2024
Herpes simplex virus spreads rapidly in human foreskin, partly driven by chemokine-induced redistribution of Nectin-1 on keratinocytes.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Comparative analysis of varicella-zoster virus and herpes simplex virus 1 interaction with epidermal terminal differentiation in primary human keratinocytes models of differentiation.bioRxiv : the preprint server for biology · 2026Article
- Pseudorabies virus induces ferroptosis by disrupting iron homeostasis through activation of TfR1 and ferritinophagy.Journal of virology · 2025Article
- Herpes simplex virus type-1 infection and spread in a novel porcine corneal explant model is restricted to the epithelium.PLoS pathogens · 2025Article
- Herpes simplex virus assembly and spread in murine skin after infection from the outside.Journal of virology · 2025Article
- Tackling cutaneous herpes simplex virus disease with topical immunomodulators-a call to action.Clinical microbiology reviews · 2025Review
- The placental battlefield: viral strategies and immune countermeasures.Frontiers in immunology · 2025Review
- Breaching the Barrier: Investigating Initial Herpes Simplex Viral Infection and Spread in Human Skin and Mucosa.Viruses · 2024Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
HSV infects keratinocytes in the epidermis of skin via nectin-1. We established a human foreskin explant infection model to investigate HSV entry and spread. HSV1 entry could only be achieved by the topical application of virus via high density microarray projections (HD-MAPs) to the epidermis, which penetrated beyond one third of its thickness, simulating in vivo microtrauma. Rapid lateral spread of HSV1 to a mean of 13 keratinocytes wide occurred after 24 hours and free virus particles were observed between keratinocytes, consistent with an intercellular route of spread. Nectin-1 staining was markedly decreased in foci of infection in the epidermis and in the human keratinocyte HaCaT cell line. Nectin-1 was redistributed, at the protein level, in adjacent uninfected cells surrounding infection, inducible by CCL3, IL-8 (or CXCL8), and possibly CXCL10 and IL-6, thus facilitating spread. These findings provide the first insights into HSV1 entry and spread in human inner foreskin in situ.
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