Homodimerization of Marek's disease virus-encoded meq protein is not sufficient for transformation of lymphocytes in chickens

Paulette F. Suchodolski, Yoshihiro Izumiya, Blanca Lupiani, Dharani K. Ajithdoss, Oren Gilad, Lucy F. Lee, Hsing-Jien Kung, Sanjay M. Reddy

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

Marek's disease virus (MDV), the etiologic agent of Marek's disease, is a potent oncogenic herpesvirus. MDV is highly contagious and elicits a rapid onset of malignant T-cell lymphomas in chickens within several weeks after infection. MDV genome codes an oncoprotein, Meq, which shares resemblance with the Jun/Fos family of bZIP transcription factors. Similar to Jun, the leucine zipper region of Meq allows the formation of homoand heterodimers. Meq homo- and heterodimers have different DNA binding affinities and transcriptional activity; therefore, they may differentially regulate transcription of viral and cellular genes. In this study we investigated the role of Meq homodimers in the pathogenicity of MDV by generating a chimeric meq gene, which contains the leucine zipper region of the yeast transcription factor GCN4 (meqGCN). A recombinant virus (rMd5-MeqGCN) containing the chimeric meqGCN gene in place of parental meq was generated with overlapping cosmid clones of Md5, a very virulent MDV strain. The rMd5-MeqGCN virus replicated in vitro and in vivo but was unable to transform T cells in infected chickens. These data provide the first in vivo evidence that Meq homodimers are not sufficient for MDV-induced transformation.

Original languageEnglish (US)
Pages (from-to)859-869
Number of pages11
JournalJournal of Virology
Volume83
Issue number2
DOIs
StatePublished - Jan 2009

ASJC Scopus subject areas

  • Immunology
  • Virology

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