Publication Database

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

Bandzählung: 22

Heftzählung: 5

Seiten: 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
14163 Berlin
+49 30 838 51833
virologie@vetmed.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.