Varicella-zoster virus is an alpha-herpesvirus that causes varicella and zoster. Infection of T cells allows VZV transfer from the respiratory tract to skin and the typical herpes zoster rash results from axonal transport after VZV reactivation in neurons. Our research program investigates the mechanisms of VZV take-over of its target cells, focusing on infection of primary human tonsil T cells and adult skin xenografts in the severe combined immunodeficiency (SCIO) mouse model. We plan to pursue our longstanding objective to understand of VZV pathogenesis in new directions that are designed to determine the role of activation of protein kinase R in VZV infection, the effects of complement as an innate defense against VZV infection of tonsil T cells and VZV countermeasures, and glycoprotein-mediated mechanisms of VZV entry into T cells. This work is expected to provide new knowledge about the takeover of host cell signaling pathways by VZV to support its replication, the regulation of VZV pathogenesis by innate host responses and how VZV overcomes these barriers, and the functions of VZV glycoproteins during infection of differentiated human cells, all of which are critical for VZV infection of the human host.

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National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Method to Extend Research in Time (MERIT) Award (R37)
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Special Emphasis Panel (NSS)
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Beisel, Christopher E
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Stanford University
Schools of Medicine
United States
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Zerboni, Leigh; Sung, Phillip; Sommer, Marvin et al. (2018) The C-terminus of varicella-zoster virus glycoprotein M contains trafficking motifs that mediate skin virulence in the SCID-human model of VZV pathogenesis. Virology 523:110-120
Zerboni, Leigh; Sung, Phillip; Lee, Gordon et al. (2018) Age-Associated Differences in Infection of Human Skin in the SCID Mouse Model of Varicella-Zoster Virus Pathogenesis. J Virol 92:
Sen, Nandini; Sung, Phillip; Panda, Arjun et al. (2018) Distinctive Roles for Type I and Type II Interferons and Interferon Regulatory Factors in the Host Cell Defense against Varicella-Zoster Virus. J Virol 92:
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Yang, Edward; Arvin, Ann M; Oliver, Stefan L (2017) The Glycoprotein B Cytoplasmic Domain Lysine Cluster Is Critical for Varicella-Zoster Virus Cell-Cell Fusion Regulation and Infection. J Virol 91:
Fran├žois, Sylvie; Sen, Nandini; Mitton, Bryan et al. (2016) Varicella-Zoster Virus Activates CREB, and Inhibition of the pCREB-p300/CBP Interaction Inhibits Viral Replication In Vitro and Skin Pathogenesis In Vivo. J Virol 90:8686-97
Khalil, Mohamed I; Che, Xibing; Sung, Phillip et al. (2016) Mutational analysis of varicella-zoster virus (VZV) immediate early protein (IE62) subdomains and their importance in viral replication. Virology 492:82-91
Oliver, Stefan L; Yang, Edward; Arvin, Ann M (2016) Varicella-Zoster Virus Glycoproteins: Entry, Replication, and Pathogenesis. Curr Clin Microbiol Rep 3:204-215
Yang, Edward; Arvin, Ann M; Oliver, Stefan L (2016) Role for the ?V Integrin Subunit in Varicella-Zoster Virus-Mediated Fusion and Infection. J Virol 90:7567-78

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