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    Equine herpesvirus type 1 (EHV-1) utilizes microtubules, dynein, and ROCK1 to productively infect cells (2010)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Frampton, Arthur R
    Uchida, Hiroaki
    von Einem, Jens
    Goins, William F
    Grandi, Paola
    Cohen, Justus B
    Osterrieder, Nikolaus
    Glorioso, Joseph C
    Quelle
    Veterinary Microbiology; 141(1/2) — S. 12–21
    ISSN: 0378-1135
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.vetmic.2009.07.035
    Pubmed: 19713056
    Kontakt
    Institut für Virologie

    Robert-von-Ostertag-Str. 7-13
    Gebäude 35
    14163 Berlin
    +49 30 838 51833
    viro@zedat.fu-berlin.de

    Abstract / Zusammenfassung

    To initiate infection, equine herpesvirus type 1 (EHV-1) attaches to heparan sulfate on cell surfaces and then interacts with a putative glycoprotein D receptor(s). After attachment, virus entry occurs either by direct fusion of the virus envelope with the plasma membrane or via endocytosis followed by fusion between the virus envelope and an endosomal membrane. Upon fusion, de-enveloped virus particles are deposited into the cytoplasm and travel to the nucleus for viral replication. In this report, we examined the mechanism of EHV-1 intracellular trafficking and investigated the ability of EHV-1 to utilize specific cellular components to efficiently travel to the nucleus post-entry. Using a panel of microtubule-depolymerizing drugs and inhibitors of microtubule motor proteins, we show that EHV-1 infection is dependent on both the integrity of the microtubule network and the minus-end microtubule motor protein, dynein. In addition, we show that EHV-1 actively induces the acetylation of tubulin, a marker of microtubule stabilization, as early as 15 min post-infection. Finally, our data support a role for the cellular kinase, ROCK1, in virus trafficking to the nucleus.