Abstract
One of the central questions of Epstein-Barr (EB) virus biology concerns the nature of the asymptotic carrier state1,2 whereby the virus, which in vitro transforms B cells into permanent lymphoblastoid cell lines with such efficiency3,4, is harboured for life in the B lymphoid tissues of all previously-infected (seropositive) individuals5. It seems highly probable that this persistent infection is primarily controlled by memory T cells (cytotoxic precursors) specifically primed to the EB virus-induced lymphocyte-detected membrane antigen LYDMA6–9. Thus the degree to which the infection can progress without interruption in individual B cells of the immune host will depend upon the timing of LYDMA expression relative to that of other viral gene functions. We now demonstrate that during EB virus-induced B cell transformation in vitro LYDMA is expressed on the cell surface soon after the appearance of the virus-associated nuclear antigen EBNA10 and coincident with, but not dependent upon, the initiation of cellular DNA synthesis. This suggests that in the lymphoid tissues of the infected host, immunological control over virus-B cell interactions can be exercised early in the cycle at the very onset of virus-induced cell proliferation.
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