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Dissecting the Molecular Mechanisms of the Tropism of Varicella-Zoster Virus for Human T Cells

Overview
Journal J Virol
Date 2016 Jan 22
PMID 26792747
Citations 13
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Abstract

Studies of varicella-zoster virus (VZV) tropism for T cells support their role in viral transport to the skin during primary infection. Multiparametric single-cell mass cytometry demonstrates that, instead of preferentially infecting skin-homing T cells, VZV alters cell signaling and remodels surface proteins to enhance T cell skin trafficking. Viral proteins dispensable in skin, such as that encoded by open reading frame 66, are necessary in T cells. Interference with VZV T cell tropism may offer novel strategies for drug and vaccine design.

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