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

Nandini Sen; Ann M Arvin

doi:10.1128/JVI.03375-14

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

J Virol. 2016 Jan 20;90(7):3284-7. doi: 10.1128/JVI.03375-14.

Authors

Nandini Sen¹, Ann M Arvin²

Affiliations

¹ Departments of Pediatrics and Microbiology & Immunology, Stanford University, Stanford, California, USA.
² Departments of Pediatrics and Microbiology & Immunology, Stanford University, Stanford, California, USA aarvin@stanford.edu.

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.

Publication types

Research Support, N.I.H., Extramural
Review

MeSH terms

Chickenpox / virology*
Exanthema / virology
Herpes Zoster / virology*
Herpes Zoster Vaccine / immunology
Herpesvirus 3, Human / genetics
Herpesvirus 3, Human / immunology*
Humans
Open Reading Frames / genetics
Signal Transduction
Skin / pathology
Skin / virology*
T-Lymphocytes / immunology
T-Lymphocytes / virology*
Tropism

Substances

Herpes Zoster Vaccine

Abstract

Publication types

MeSH terms

Substances

Grants and funding