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Modeling the pathology, immune responses, and kinetics of HSV-1 replication in the lip scarification model
Journal article   Open access   Peer reviewed

Modeling the pathology, immune responses, and kinetics of HSV-1 replication in the lip scarification model

Kevin P. Egan, Alexander G. Allen, Brian Wigdahl and Stephen R. Jennings
Virology (New York, N.Y.), v 514, pp 124-133
15 Jan 2018
PMID: 29175626
url
https://doi.org/10.1016/j.virol.2017.11.010View
Published, Version of Record (VoR)Open Access (Publisher-Specific) Open

Abstract

Animal model Herpes simplex virus Histopathology Immune response Infection kinetics Lip scarification
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. [Display omitted] •The lip is a physiologically relevant site for studying HSV-1 infections.•Topical application of HSV-1 to a scratched lip leads to productive infection.•HSV-1 replicates in the lip prior to the TG.•The primary infection resolves after 15 days and viral genomes persist in the TG.•CD4+ and CD8+ T cells can be found in the lip and TG after resolution of primary infection.

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Collaboration types
Domestic collaboration
Web of Science research areas
Virology
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