Nevertheless, our recent preliminary finding that the ZV mutant virus is at least an order-of-magnitude defective relative to the parental WT EBV in establishing colonies of proliferating lymphocytic cells following infection of primary human B cells (Yu and Mertz, unpublished data) provides strong evidence that ZEB1 binding to the ZV element of Zp is, indeed, important for establishing a stable latent infection in B cells as well as epithelial cells. The gene discussed is ZEB1; the disease is disease arising from reactivation of latent virus.