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Nydia C De La Cruz1, Maureen Möckel1, Hanna Niehues2

  • 1Center for Biochemistry, University Hospital Cologne, University of Cologne, Cologne, Germany.

Journal of Virology
|June 8, 2023
PubMed
Summary

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Herpes simplex virus 1 (HSV-1) invasion into human skin requires overcoming epidermal barriers. Impaired tight junctions and skin barrier defects, common in atopic dermatitis, allow HSV-1 to access its receptor, nectin-1, facilitating infection.

Area of Science:

  • Virology
  • Dermatology
  • Cell Biology

Background:

  • Herpes simplex virus 1 (HSV-1) infects human epithelia by accessing keratinocyte receptors.
  • Nectin-1 is an efficient HSV-1 receptor but is typically inaccessible in healthy human epidermis.
  • Atopic dermatitis features impaired skin barrier functions, potentially creating entry points for HSV-1.

Purpose of the Study:

  • To investigate how epidermal barrier integrity influences HSV-1 invasion.
  • To determine the impact of barrier defects on nectin-1 accessibility for HSV-1.
  • To explore the role of tight junctions and inflammatory cytokines in HSV-1 skin entry.

Main Methods:

  • Utilized human epidermal equivalents to model skin barrier formation and viral invasion.
  • Analyzed the correlation between tight junction formation and HSV-1 infection rates.
Keywords:
HSV-1IL-4/IL-13N/TERT-1 cellsepidermal barriersepidermal equivalentshuman keratinocyteshuman skinnectin-1nonlesional atopic dermatis keratinocytesnonlesional atopic dermatitis skinprimary human keratinocytestight junctionsvirus entry

Related Experiment Videos

  • Examined nectin-1 distribution in healthy, atopic dermatitis, and cytokine-treated human epidermis.
  • Assessed the effect of interleukin 4 (IL-4) and IL-13 on epidermal barrier function and HSV-1 susceptibility.

    • Main Results:

    • Mature tight junctions in healthy epidermis prevent HSV-1 access to nectin-1.
    • Impaired epidermal barriers, induced by IL-4/IL-13 or present in atopic dermatitis keratinocytes, correlated with increased HSV-1 infection.
    • Nectin-1 is distributed throughout epidermal layers, localized beneath tight junctions.
    • In atopic dermatitis and IL-4/IL-13-treated skin, defective tight junctions facilitate nectin-1 accessibility for HSV-1.

    Conclusions:

    • Functional tight junctions are critical for preventing HSV-1 entry into human epidermis.
    • Defective epidermal barriers, including compromised tight junctions and stratum corneum, are essential for HSV-1 skin invasion.
    • Nectin-1 accessibility to HSV-1 is significantly enhanced by inflammation-induced barrier defects, as seen in atopic dermatitis.