Gr-1+ cells, but not neutrophils, limit virus replication and lesion development following flank infection of mice with herpes simplex virus type-1

Magdalena Wojtasiak, Danielle Pickett, Michelle Tate, Sammy Bedoui, Emma Job, Paul Whitney, Andrew Brooks, Patrick Reading

Research output: Contribution to journalArticleResearchpeer-review

23 Citations (Scopus)

Abstract

Neutrophils are prominent in epidermal and dermal layers of human herpetic lesions and are rapidly recruited into the skin follow epidermal abrasion and infection of mice with herpes simplex virus type-1 (HSV-1). Herein, we demonstrate that early production of neutrophil-attracting chemokines KC/MIP-2 is associated with transient recruitment of neutrophils into the skin of HSV-1-infected mice in temporal association with the development of herpetic lesions. Treatment of HSV-1-infected mice with a Ly6G-specific mAb induced systemic neutropenia, but surprisingly did not alter virus replication or lesion development. In contrast, depletion of Gr-1(+) cells with mAb RB6-8C5 led to enhanced virus growth and lesion severity. Thus, while neutrophils are prominent in zosteriform lesions of HSV-1-infected mice, they do not appear to play a major role in controlling virus replication or lesion development and/or healing. In contrast, Gr-1(+) cells limit both virus replication and lesion development in the zosteriform model.
Original languageEnglish
Pages (from-to)143 - 151
Number of pages9
JournalVirology
Volume407
Issue number1
DOIs
Publication statusPublished - 2010
Externally publishedYes

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