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    The Role of Human Cytomegalovirus Protein UL135 in Virus Replication, Latency, and Reactivation

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    Author
    Rak, Michael A.
    Issue Date
    2018
    Keywords
    Abi-1
    CIN85
    Cytomegalovirus
    Latency
    Reactivation
    UL135
    Advisor
    Goodrum, Felicia D.
    
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    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Human cytomegalovirus (CMV) is a ubiquitous herpesvirus that infects the majority of the world’s population. CMV can establish a latent infection, enabling the lifelong persistence of CMV infection and effectively evading the immune system and antiviral drugs. We have characterized the protein product of UL135 (pUL135), and discovered that pUL135 drives viral replication and is necessary for viral reactivation from latency, counteracting the latency-promoting effects of another CMV protein, pUL138. The functions of pUL135 and pUL138 proteins are antagonistic, epistatically linked, and the balance between pUL135 and pUL138 regulates viral infection and latency. Through the use of proteomic screens, we have identified and disrupted interactions of pUL135 with cellular proteins Abi-1 and CIN85; we discovered that interactions are necessary for viral reactivation from latency. pUL135 and its interactions with Abi-1 and CIN85 influence the levels of EGFR on the cell and alter the dynamics of EGFR trafficking within the cell. This work investigates the various roles and mechanisms by which UL135 serves as a mediator of CMV infection.
    Type
    text
    Electronic Dissertation
    Degree Name
    Ph.D.
    Degree Level
    doctoral
    Degree Program
    Graduate College
    Cellular and Molecular Medicine
    Degree Grantor
    University of Arizona
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