HUMAN-HERPESVIRUS-6 VARIANT-A, BUT NOT VARIANT-B, INFECTS EBV-POSITIVE B-LYMPHOID-CELLS, ACTIVATING THE LATENT EBV GENOME THROUGH A BZLF-1-DEPENDENT MECHANISM

Human herpesvirus 6, a predominantly T lymphotropic virus, has been re cently shown to infect some EBV-positive B cell lines, and to induce i n them the activation of the EBV lytic cycle. Here we have confirmed a nd extended such observations, showing that (1) this phenomenon is res tricted to the variant A of HHV-6: in fact two isolates belonging to t he HHV-6 variant B (BA92 and Z29) were neither able to infect any B ce ll line, independently of the EBV status, nor to induce the EBV genome expression. The only exception is represented by the P3HR1 cells, in which, however, the infection by the variant B does not determine indu ction of EBV antigens; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection, increasi ng the binding sites and the percentage of infectable cells, as detect ed by immunoelectron microscopy; and (3) HHV-6 infected T cells, trans fected with plasmids bearing the promoter regions of the EBV early gen es BZLF1 and BMRF1, show a strong transactivation of these promoters.