Abstract

The lip scarification model of herpes simplex virus type 1 (HSV-1) infection can be used to study acute infection in the orofacial tissue and the establishment of viral latency. In this study, mice were inoculated with HSV-1 and tissue harvested during the acute phase of infection. Clinical presentation of classical open sores on the lip of infected mice was observed. We defined the histopathology, disease scores, and immune infiltration of the lower lip during the formation and resolution of the clinical lesions. Finally, the kinetics of virus replication and transport of viral genomes to the trigeminal ganglia were established. With the virological and pathologic events of acute infection defined, the HSV-1 lip scarification model can now be used to study primary HSV-1 infection, invasion of the trigeminal ganglia, and establishment of latency.

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