The oncogenic associations with Epstein-Barr Virus (EBV), a member of the Herpesviridae family, have been studied in great detail. But key pieces of information are still missing. What exactly does EBV do to cause cancer? What molecular mechanism does it work by?
A collaboration between Henri-Jacques Delecluse and Ingrid Hoffmann, researchers at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DFKZ) has uncovered a potential lead. The viral protein BNRF1 induces constitutive formation of spindle poles, or centromeres. The consequence is that, during mitosis, when chromosomes should make copies of themselves and then split into different cells, chromosomes divide unequally. This increases the risk for cancer, as unequal division of chromosomes can lead to mutations.
To study this, the cancer researchers synthesized BNRF1-deficient EBV and observed that the heightened number of spindle fibers was no longer present in infected cells.
BNRF-1 is present in an infectious EBV particle. This means that the EBV genome is technically not needed for oncogenesis. The finding suggests that a vaccine is much-needed, as a successful vaccine would allow the formation of memory antibodies that can neutralize infectious particles.
Press Release from the DFKZ:
-- Sharon Kam