Abstract
During primary infection, herpes simplex virus 1 (HSV-1) enters human skin or mucosa and establishes lifelong latency in sensory neurons. The skin is normally well protected from invading pathogens as the epithelium forms effective barriers. How HSV-1 can overcome this barrier in vivo remains to be shown. One prominent example for successful HSV-1 skin invasion is eczema herpeticum, a disseminated HSV-1 infection and severe complication of atopic dermatitis (AD). In lesional skin of AD patients, the mechanical skin barrier consisting of the stratum corneum and tight junctions in the stratum granulosum is impaired.
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