Varicella-zoster virus retains major histocompatibility complex class I proteins in the Golgi compartment of infected cells.
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Selective retention of herpes simplex virus-specific T cells in latently infected human trigeminal gangliaA comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivationViral inhibition of the transporter associated with antigen processing (TAP): a striking example of functional convergent evolutionVaricelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processingMicroarray analysis of host cell gene transcription in response to varicella-zoster virus infection of human T cells and fibroblasts in vitro and SCIDhu skin xenografts in vivoVaricellovirus UL 49.5 proteins differentially affect the function of the transporter associated with antigen processing, TAP.The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3Varicella-Zoster virus pathogenesis and immunobiology: new concepts emerging from investigations with the SCIDhu mouse model.Varicella-zosterT-cell tropism and the role of ORF66 protein in pathogenesis of varicella-zoster virus infectionCharacterization of the host immune response in human Ganglia after herpes zoster.Novel Nipah virus immune-antagonism strategy revealed by experimental and computational study.Varicella-zoster virus (VZV) ORF17 protein induces RNA cleavage and is critical for replication of VZV at 37 degrees C but not 33 degrees C.The capacity of UL49.5 proteins to inhibit TAP is widely distributed among members of the genus Varicellovirus.Simian varicella virus pathogenesis.ORF66 protein kinase function is required for T-cell tropism of varicella-zoster virus in vivoReview: The neurobiology of varicella zoster virus infection.Simian varicella virus gene expression during acute and latent infection of rhesus macaques.Varicella-Zoster Virus and Herpes Simplex Virus 1 Differentially Modulate NKG2D Ligand Expression during Productive Infection.Human herpesviridae methods of natural killer cell evasionVaricella-zoster virus modulates NF-kappaB recruitment on selected cellular promotersVaricella-zoster virus transfer to skin by T Cells and modulation of viral replication by epidermal cell interferon-alphaAge and immune status of rhesus macaques impact simian varicella virus gene expression in sensory gangliaT-cell immunity to human alphaherpesviruses.Humoral and cellular immunity to varicella-zoster virus: an overview.Varicella-Zoster Virus Downregulates Programmed Death Ligand 1 and Major Histocompatibility Complex Class I in Human Brain Vascular Adventitial Fibroblasts, Perineurial Cells, and Lung FibroblastsClinical and molecular aspects of varicella zoster virus infection.Varicella zoster virus immune evasion strategies.Varicella-zoster virus open reading frame 66 protein kinase and its relationship to alphaherpesvirus US3 kinases.VZV infection of keratinocytes: production of cell-free infectious virions in vivoViral serine/threonine protein kinasesExploiting human herpesvirus immune evasion for therapeutic gain: potential and pitfalls.Molecular studies of the Oka varicella vaccine.Clinical and molecular aspects of the live attenuated Oka varicella vaccine.Cytomegalovirus immune evasion by perturbation of endosomal trafficking.Persistent high frequencies of varicella-zoster virus ORF4 protein-specific CD4+ T cells after primary infectionEquine herpesvirus type 4 UL56 and UL49.5 proteins downregulate cell surface major histocompatibility complex class I expression independently of each other.The alphaherpesvirus US3/ORF66 protein kinases direct phosphorylation of the nuclear matrix protein matrin 3Varicella-zoster virus productively infects mature dendritic cells and alters their immune function.Downregulation of class I major histocompatibility complex surface expression by varicella-zoster virus involves open reading frame 66 protein kinase-dependent and -independent mechanisms.
P2860
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P2860
Varicella-zoster virus retains major histocompatibility complex class I proteins in the Golgi compartment of infected cells.
description
2001 nî lūn-bûn
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2001 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի մայիսին հրատարակված գիտական հոդված
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2001年の論文
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2001年学术文章
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2001年学术文章
@zh-cn
2001年学术文章
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2001年学术文章
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2001年学术文章
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2001年學術文章
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name
Varicella-zoster virus retains ...... compartment of infected cells
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Varicella-zoster virus retains ...... compartment of infected cells.
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Varicella-zoster virus retains ...... compartment of infected cells.
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Varicella-zoster virus retains ...... compartment of infected cells
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Varicella-zoster virus retains ...... compartment of infected cells.
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Varicella-zoster virus retains ...... compartment of infected cells.
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Varicella-zoster virus retains ...... compartment of infected cells
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Varicella-zoster virus retains ...... compartment of infected cells.
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Varicella-zoster virus retains ...... compartment of infected cells.
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P2093
P2860
P1433
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Varicella-zoster virus retains ...... compartment of infected cells.
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P2093
P2860
P304
P356
10.1128/JVI.75.10.4878-4888.2001
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P577
2001-05-01T00:00:00Z