One of the hallmarks of oncogenic viruses is their ability to subvert the growth regulation and evade immune response of the host. There are a number of tricks devised by various virus families. Oncogenic herpesviruses often accomplish this by encoding homologs of cellular genes involved in these functions. These viral homologs sometimes are hyperactive forms of their cellular counterparts, which function to overtake the cellular pathways, other times serve as decoys to mask the cellular functions. Marek's disease virus (MDV) carries at least two genes in that category. We have previously described Meq protein (MEQ gene product), a transcriptional factor with homology to proto-oncogenes Jun and Fos in the bZIP domain. Meq dimerizes with Jun or Fos and the Meq/Jun heterodimer is able to transactivate promoters with AP-1 site. We show here that Meq and Jun colocalize in living cells, adding to the physiological significance of the dimer formation. In addition, we present data to show that Meq and Jun can functionally complement each other in cis and in trans, using transformation and transactivation assays. Finally we describe the discovery of an IL8 ehemokine homolog, designated as v-IL8 (viral IL8) in the MDV genome and discuss its possible function in MDV infection.
|Number of pages||8|
|Publication status||Published - Apr 1 1999|
- Herpesviral oncogene
ASJC Scopus subject areas