Biological data are accumulating on a repertoire of EBV genes and molecular mechanisms by which the productive cycle is reactivated in latently infected epithelial cells, as well as the mechanisms by which reactivation can be suppressed.ĭuring epithelial differentiation, major changes take place in the gene expression and morphology of the differentiating cells. While much investigation has sought to elucidate EBV's role in the immortalization and transformation of B lymphocytes, little is known about the molecular mechanisms underlying EBV's lytic infection of epithelial cells. EBV-infected B lymphocytes from the peripheral blood or in vitro infected B lymphocytes can proliferate continuously in culture. EBV is also associated with human malignancies, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and B and T cell lymphomas in immunocompromized individuals (for reference, see Rickinson and Kieff 1996). In the oral epithelium, EBV replication is observed primarily in the upper spinous layer that consists of the terminally differentiated nondividing cells. EBV replication is highly dependent on the state of cell differentiation. Transmission by oral contact results in infection of the oral and/or nasopharyngeal epithelium, and subsequent infection of B lymphocytes in the adjacent lymphoid tissue ensues. We designated this novel ubiquitously expressed nuclear protein as ubinuclein and the corresponding gene as UBN1.Įpstein-Barr virus (EBV) is a human herpes virus that persists in latency for the lifetime of the infected host. The gene was identified in tail-to-tail orientation with the periplakin gene ( PPL) in human chromosome 16p13.3 and in a syntenic region in mouse chromosome 16. The overexpression of tagged cDNA constructs in keratinocytes revealed that the NH 2 terminus is essential for the nuclear localization, while the central domain is responsible for the interaction with EB1 and for the phenotype of transfected keratinocytes similar to terminal differentiation. The transcript is present in a wide variety of human adult, fetal, and tumor tissues, and the protein is detected in the nuclei throughout the human epidermis and as either grainy or punctuate nuclear staining in the cultured keratinocytes. Here, we characterize a novel cellular protein interacting with the basic domains of EB1 and c-Jun, and competing of their binding to the AP1 consensus site. The product of the EBV BZLF1 early gene, EB1, a member of the basic leucine-zipper family of transcription factors, interacts with both viral and cellular promoters and transcription factors, modulating the reactivation of latent EBV infection. The major target tissues for Epstein-Barr virus (EBV) infection are B lymphocytes and epithelial cells of the oropharyngeal zone.
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