Upregulation of CXCL10 in human dorsal root ganglia during experimental and natural varicella-zoster virus infection

Megan Steain; Kavitha Gowrishankar; Michael Rodriguez; Barry Slobedman; Allison Abendroth

doi:10.1128/JVI.01816-10

Upregulation of CXCL10 in human dorsal root ganglia during experimental and natural varicella-zoster virus infection

Megan Steain, Kavitha Gowrishankar, Michael Rodriguez, Barry Slobedman, Allison Abendroth^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

44 Citations (Scopus)

Abstract

Varicella-zoster virus (VZV) reactivation causes herpes zoster, which is accompanied by an influx of lymphocytes into affected ganglia, but the stimulus for this infiltrate is not known. We report that VZV infection of ganglia leads to increased CXCL10 production in vitro, in an explant ganglion model and in naturally infected dorsal root ganglia (DRG) during herpes zoster. Lymphocytes expressing the receptor for CXCL10, CXCR3, were also observed throughout naturally infected ganglia during herpes zoster, including immediately adjacent to neurons. This study identifies VZV-induced CXCL10 as a potential driver of T lymphocyte recruitment into DRG during herpes zoster.

Original language	English
Pages (from-to)	626-631
Number of pages	6
Journal	Journal of Virology
Volume	85
Issue number	1
DOIs	https://doi.org/10.1128/JVI.01816-10
Publication status	Published - Jan 2011
Externally published	Yes

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abstract = "Varicella-zoster virus (VZV) reactivation causes herpes zoster, which is accompanied by an influx of lymphocytes into affected ganglia, but the stimulus for this infiltrate is not known. We report that VZV infection of ganglia leads to increased CXCL10 production in vitro, in an explant ganglion model and in naturally infected dorsal root ganglia (DRG) during herpes zoster. Lymphocytes expressing the receptor for CXCL10, CXCR3, were also observed throughout naturally infected ganglia during herpes zoster, including immediately adjacent to neurons. This study identifies VZV-induced CXCL10 as a potential driver of T lymphocyte recruitment into DRG during herpes zoster.",

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AU - Slobedman, Barry

AU - Abendroth, Allison

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AB - Varicella-zoster virus (VZV) reactivation causes herpes zoster, which is accompanied by an influx of lymphocytes into affected ganglia, but the stimulus for this infiltrate is not known. We report that VZV infection of ganglia leads to increased CXCL10 production in vitro, in an explant ganglion model and in naturally infected dorsal root ganglia (DRG) during herpes zoster. Lymphocytes expressing the receptor for CXCL10, CXCR3, were also observed throughout naturally infected ganglia during herpes zoster, including immediately adjacent to neurons. This study identifies VZV-induced CXCL10 as a potential driver of T lymphocyte recruitment into DRG during herpes zoster.

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Upregulation of CXCL10 in human dorsal root ganglia during experimental and natural varicella-zoster virus infection

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