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

Amy C. Keller, Hussain Badani, P. Mason McClatchey, Nicholas L. Baird, Jacqueline L. Bowlin, Ron Bouchard, Guey Chuen Perng, Jane E.B. Reusch, Benedikt B. Kaufer, Don Gilden, Aamir Shahzad, Peter G.E. Kennedy, Randall J. Cohrs

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)674-682
Number of pages9
JournalJournal of NeuroVirology
Issue number5
Publication statusPublished - 2016 Oct 1

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Virology


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