Efficient EBV superinfection of group I Burkitt's lymphoma cells distinguishes requirements for expression of the Cp viral promoter and can activate the EBV productive cycle.

Group I Burkitt's lymphoma cell lines conditionally expressing the CD21 receptor for EBV infection were superinfected with EBV. The incoming EBV entered its normal program of gene expression, producing EBNA-2 and LMP-1 and activating the Cp EBNA promoter, but the endogenous virus in the BL lines was not induced to express EBNA-2 or transcribe RNA from Cp. LMP-1 was, however, expressed from the endogenous genome in response to superinfection. In a proportion of the superinfected Akata cells, the productive cycle antigen BZLF1 was induced and the ability of infecting virus to cause this was sensitive to inactivation by uv light. The results show that the restricted latent pattern of EBV gene expression observed in Group I BL cells is not a consequence of lack of appropriate transcription factor activity but results from inactivation of part of the viral genome, probably by methylation. Induction of BZLF1 in some of the cells also indicates a novel pathway for activation of the virus productive cycle.