Hypoxia treatment not only increased the expression of the EBV immediate-early protein Zta (which mediates the switch between the latent and lytic form of infection), but also increased the number of EBV DNA copies in B95-8 cells.
EBV in latent infection can be activated to lytic infection by hypoxia treatment.
One such virus that displays this characteristic is the lymphotropic human herpesvirus, Epstein-Barr virus (EBV). EBV is latent in B-cells that exist in the peripheral circulation as non-dividing memory B-cells; within lymph nodes EBV-infected cells become proliferating blasts that secrete antibody [19,20] . These two dramatically distinct cellular phenotypes result from two different viral gene expression patterns during latency [ibid]. Recent results indicate that the EBV transactivator, Epstein-Barr nuclear antigen 1 (EBNA1), is regulated by oxygen tension  . Under hypoxic or reducing conditions, EBNA1 is active as a transactivator and drives viral gene expression required for cell proliferation. For EBNA1, the redox state of a pair of cysteines in a conserved cys-x-x-cys motif governs its ability to transactivate
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