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    Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology (2016)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Keller, Amy C
    Badani, Hussain
    McClatchey, P Mason
    Baird, Nicholas L
    Bowlin, Jacqueline L
    Bouchard, Ron
    Perng, Guey-Chuen
    Reusch, Jane E B
    Kaufer, Benedikt B (WE 5)
    Gilden, Don
    Shahzad, Aamir
    Kennedy, Peter G E
    Cohrs, Randall J
    Quelle
    Journal of neurovirology; 22(5) — S. 674–682
    ISSN: 1355-0284
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://link.springer.com/article/10.1007/s13365-016-0457-0
    DOI: 10.1007/s13365-016-0457-0
    Pubmed: 27245593
    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

    Varicella zoster virus (VZV) is a ubiquitous alphaherpesvirus that establishes latency in ganglionic neurons throughout the neuraxis after primary infection. Here, we show that VZV infection induces a time-dependent significant change in mitochondrial morphology, an important indicator of cellular health, since mitochondria are involved in essential cellular functions. VZV immediate-early protein 63 (IE63) was detected in mitochondria-rich cellular fractions extracted from infected human fetal lung fibroblasts (HFL) by Western blotting. IE63 interacted with cytochrome c oxidase in bacterial 2-hybrid analyses. Confocal microscopy of VZV-infected HFL cells at multiple times after infection revealed the presence of IE63 in the nucleus, mitochondria, and cytoplasm. Our data provide the first evidence that VZV infection induces alterations in mitochondrial morphology, including fragmentation, which may be involved in cellular damage and/or death during virus infection.