Entry Mechanisms of Herpes Simplex Virus 1 into Murine Epidermis: Involvement of Nectin-1 and Herpesvirus Entry Mediator as Cellular Receptors

What is it about?

Herpes simplex virus (HSV) can cause a range of diseases in humans from uncomplicated mucocutaneous lesions to life-threatening infections. The skin is one target tissue of HSV and the question of how the virus overcomes the protective skin barrier and penetrates into the tissue to reach its receptors is still open. Which are the cell surface molecules that act as receptors for HSV in skin? From various studies in cell lines, we know that the herpesvirus entry mediator (HVEM) and nectin-1 can interact with the viral envelope protein gD, which in turn leads to fusion of the viral envelope with cellular membranes. To explore the contributions of HVEM and nectin-1 to uptake into skin, we used nectin-1 or HVEM-deficient mice and performed ex vivo infection studies. Our results demonstrate that HSV entry into murine epidermis strongly depends on the presence of nectin-1, but HVEM can potentially replace nectin-1 as a receptor. This approach allows us to transfer our knowledge of virus entry mechanisms resulting from studies in cell lines into an understanding of how HSV enters its natural target tissues.

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