Biologic activities of extracellular EpsteinBarr virus (EB virus) from two laboratory strains, namely, PJ-HR-I (P-H) from Burkitt lymphoma and B95-8 (B95) from infectious mononucleosis, were compared. Virus stocks from both sources contained approximately the same number of virions. Virus from the P-H line induced "early antigen" in six nonproducer EB virus genome carrier cell lines; virus from B95 did not induce "early antigen." Extracellular virus from B95 regularly caused lymphocytes from human umbilical cords to form continuous lines (immortalization); P-H virus did not cause primary cultures of human lymphocytes to grow continuously. B95 virus stimulated DNA synthesis as determined by rate of incorporation of [3H]thymidine into acid-insoluble material; P-H virus did not stimulate DNA synthesis. Pretreatment of lymphocytes with undiluted P-H virus inhibited immortalization and stimulation of DNA synthesis by B95 virus. The inhibitory properties of the P-H virus were sedimented at 100,000 X g and inactivated by heat and UV irradiation; interference by the P-H virus was neutralized by human serum with antibody to EB virus and not by antibody-negative human serum.The hypothesis most consistent with these results is that the P-H virus is defective in gene(s) needed for initiation of immortalization. We speculate that the absence of this gene allows early antigen to be expressed upon superinfection of nonproducer cell lines. The availability of two laboratory strains of EB virus which differ in biologic behavior provides starting material for analysis of the mechanism of lymphocyte immortalization by EB virus and of virus structural differences which affect immortalization.Two biologic properties of Epstein-Barr virus (EB virus) can be studied in cell culture systems. The first is transformation or, as we prefer, immortalization (1-4). The virus causes normal human lymphocytes with a limited life span in vitro to form continuous cell lines. The second activity is abortive replication. When EB virus is added to certain continuous human lymphoblastoid cell lines, an EB virus associated antigen complex termed "early antigen" (EA) appears (5). The term "early antigen" is used because superinfected cells do not produce mature virus and because production of "early antigen" occurs in the presence of levels of cytosine arabinoside which inhibit DNA synthesis (6). However, abortive infection and the appearance of early antigen are accompanied by inhibition of cell DNA synthesis (7) and by impaired ability of the superinfected cells to form colonies in soft agar (8). A major obstacle to comparative study of EB virus strains has been that most producer cell lines release minute quantities of extra-cellular virus, and there is yet no completely permissive culture system. For most studies heretofore, purified extracellular EB virions and EB viral DNA have been prepared from the P3J-HR-1 line of Burkitt lymphoma cells (9, 10). Recently it was demonstrated that high titers of EB virus, biologically active by the immort...

The presence of antibodies to a KSHV antigenic peptide correlates with the presence of Kaposi's sarcoma in a high-risk population and provides further evidence of an etiologic role for KSHV.

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An Epstein-Barr viral gene (ZEBRA) is identified that, in human lymphoblastoid cells, activates a switch causing the virus to shift from the latent to the replicative phase of its life cycle. We have shown that a 2.7-kilobase-pair rearranged Epstein-Barr virus DNA fragment of this gene (BamHI fragment WZhet) induced transient expression of viral replicative antigens and polypeptides when it was transfected into a somatic cell hybrid, which was derived from the fusion of an epithelial line cell with a Burkitt lymphoma cell. We now show that this rearranged WZhet fragment, when introduced stably into lymphoblastoid cells, will activate expression of the complete viral replicative cycle in 1-10% of the lymphoblastoid cells, leading to production of biologically active virions that can immortalize primary lymphocytes. The transfected plasmid appears to be regulated in a manner analogous to the complete Epstein-Barr virus genome.