title: Dissecting the Molecular Mechanisms of the Tropism of Varicella-Zoster Virus for Human T Cells.
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.
authors.affiliation: Departments of Pediatrics and Microbiology & Immunology, Stanford University, Stanford, California, USA.
authors.forename: Nandini
authors.initials: N
authors.lastname: Sen
authors.affiliation: Departments of Pediatrics and Microbiology & Immunology, Stanford University, Stanford, California, USA aarvin@stanford.edu.
authors.forename: Ann M
authors.initials: AM
authors.lastname: Arvin
mesh_terms: D002644:Chickenpox / Q000821:virology*; D005076:Exanthema / Q000821:virology; D006562:Herpes Zoster / Q000821:virology*; D053061:Herpes Zoster Vaccine / Q000276:immunology; D014645:Herpesvirus 3, Human / Q000235:genetics / Q000276:immunology*; D006801:Humans; D016366:Open Reading Frames / Q000235:genetics; D015398:Signal Transduction; D012867:Skin / Q000473:pathology / Q000821:virology*; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology*; D018523:Tropism
chemical_list: D053061:Herpes Zoster Vaccine