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MEQ and V-IL8: cellular genes in disguise?
1Department of Molecular Biology and Microbiology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4960, USA.
Acta Virologica
|March 4, 2000
Summary
Marek's disease virus (MDV) encodes Meq protein, a viral oncoprotein that dimerizes with host transcription factors Jun and Fos. This study demonstrates Meq and Jun functionally complement each other, impacting viral oncogenesis and immune evasion.
Area of Science:
- Virology
- Molecular Biology
- Oncology
Background:
- Oncogenic viruses manipulate host cell growth and immune evasion.
- Herpesviruses encode viral homologs of cellular genes to achieve this.
- Marek's disease virus (MDV) utilizes such strategies, including the Meq protein.
Purpose of the Study:
- To investigate the function of the MDV Meq protein, a homolog of proto-oncogenes Jun and Fos.
- To explore the interaction and functional complementation between Meq and Jun.
- To identify and characterize viral homologs of cellular immune-related genes in MDV.
Main Methods:
- Co-localization studies in living cells to observe Meq and Jun interaction.
- Transformation and transactivation assays to assess functional complementation.
- Bioinformatic analysis and characterization of viral gene homologs.
Main Results:
- Meq protein and Jun protein colocalize in living cells, confirming dimer formation.
- Meq and Jun functionally complement each other in cis and trans.
- A viral IL8 (v-IL8) chemokine homolog was identified in the MDV genome.
Conclusions:
- The Meq/Jun heterodimer plays a significant role in MDV-mediated cellular transformation and transactivation.
- Meq's interaction with Jun highlights a mechanism for subverting host cell pathways.
- The discovery of v-IL8 suggests MDV employs chemokine homologs for immune evasion.
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