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Title: MEQ AND V-IL8: CELLULAR GENES IN DISGUISE?

Author
item LIU, J - CASE WESTERN RESERVE UNIV
item LIN, S - CASE WESTERN RESERVE UNIV
item XIA, L - CASE WESTERN RESERVE UNIV
item BRUNOVSKIS, P - CASE WESTERN RESERVE UNIV
item LI, D - CASE WESTERN RESERVE UNIV
item DAVIDSON, I - KIMRON VETERINARY INST
item Lee, Lucy
item KUNG, H - CASE WESTERN RESERVE UNIV

Submitted to: Acta Virologica
Publication Type: Proceedings
Publication Acceptance Date: 6/1/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Marek's disease virus (MDV) is a herpesvirus that causes cancer-like disease in chickens. Molecular characterization of MDV is essential in order to develop successful programs for control of Marek's disease. We have characterized two MDV genes termed MEQ and VIL8. Our data showed that VIL8 produces a chemical substance that attracts certain type of immune cells in response to MDV infection. This new information is very important and should be useful to scientists in their attempts to understand the interaction between the causative virus and the host. Further, the data will help scientists in designing more effective programs for control of this economically important disease of poultry.

Technical Abstract: 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 chemokine homolog, designated as v-IL8 (viral IL8) in the MDV genome and discuss its possible function in MDV infection.