Abstract

Herpes simplex virus type 1 (HSV-1) causes recurrent mucocutaneous lesions, yet existing animal models incompletely recapitulate characteristic skin manifestations. Here, we established a mouse model of cutaneous HSV-1 infection by combining epithelial barrier disruption with localized viral inoculation. Superficial scarification of the ear followed by HSV-1 exposure resulted in consistent lesion formation. Administration of hydrocortisone further increased the incidence of lesions, highlighting the critical roles of epithelial integrity and host immune regulation in the pathogenesis of HSV-1 infection. Using this model, we evaluated the antiviral efficacy of Acyclovir. Treatment significantly reduced lesion severity, lesion size, and viral gene expression, indicating partial suppression of viral replication. Notably, acyclovir treatment was associated with increased expression of T-bet and Foxp3 in lymphoid tissues, suggesting modulation of both effector and regulatory immune responses. Collectively, this model successfully reproduces localized HSV-1 skin lesions, serving as a useful platform for investigating viral pathogenesis and evaluating antiviral therapies. However, further studies, including direct viral quantification and histopathological analysis, are required.

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