Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 204, Issue 3, Pages 595-603Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061792
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Funding
- NIAID NIH HHS [AI-30731, R37 AI042528, P01 AI030731, R01 AI050132, R21 AI050132, R01 AI042528, AI-50132, AI-42528, P30 AI027757] Funding Source: Medline
- NICHD NIH HHS [HD-051455, R01 HD051455] Funding Source: Medline
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Cytotoxic CD8(+) T cells play a critical role in controlling herpes simplex virus (HSV) infection and reactivation. However, little is known about the spatiotemporal dynamics of CD8(+) T cells during HSV lesion evolution or about their involvement in immune surveillance after lesion resolution. Using quantum dot - conjugated peptide - major histocompatibility complex multimers, we investigated the in vivo localization of HSV-2-specific CD8(+) T cells in sequential biopsies of human genital skin during acute, resolving, and healed stages of HSV-2 reactivation. Our studies revealed that functionally active CD8(+) T cells selectively infiltrated to the site of viral reactivation. After lesion healing in concert with complete reepithelialization and loss of HSV DNA from skin biopsies, HSV-2-specific CD8(+) T cells persisted for more than two months at the dermal - epidermal junction, adjacent to peripheral nerve endings. In two out of the six sequentially studied individuals, HSV-2 DNA reappeared in clinically and histologically normal - appearing skin. Detection of viral DNA was accompanied by increased numbers of both HSV-specific and total CD8(+) T cells in the dermis. These findings indicate that the frequency and clinical course of HSV-2 reactivation in humans is influenced by virus-specific CD8(+) T cells that persist in peripheral mucosa and genital skin after resolution of herpes lesions.
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