Abstract
Primary Epstein-Barr Virus (EBV) infection begins in the oropharynx where the virus establishes persistent infection of epithelial cells through continued cycles of infection, virus replication, cell death, virus release and infection of new cells. Early in primary infection, virus spreads from epithelial cells to subepithelial B lymphocytes. Infected B lymphocytes are largely non-permissive for virus replication. EBV establishes latent infection in B lymphocytes and transforms these cells so that they can secrete immunoglobulin and proliferate indefinitely in vitro. In immune deficient humans, EBV infected lymphocytes can also proliferate into malignant tumors. In latently infected B lymphocytes, EBV characteristically expresses a restricted set of virus genes which are presumed to i) maintain latent virus genome persistence, ii) cause the B lymphocyte growth transformation associated with latent viral infection and iii) represent targets for the immune response which is responsible for the prevention of outgrowth of latently infected B lymphocytes in humans.
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Liebowitz, D., Kieff, E., Sample, J., Birkenbach, M., Wang, F. (1989). Epstein-Barr Virus Transformation of B Lymphocytes: Molecular Pathogenesis. In: Ablashi, D.V., Faggioni, A., Krueger, G.R.F., Pagano, J.S., Pearson, G.R. (eds) Epstein-Barr Virus and Human Disease • 1988. Experimental Biology and Medicine, vol 20. Humana Press. https://doi.org/10.1007/978-1-4612-4508-7_1
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DOI: https://doi.org/10.1007/978-1-4612-4508-7_1
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