Expression data from CCL185 carcinoma cell line transiently infected with EBV

Epstein-Barr virus(EBV) is associated with malignancies from lymphoid and epithelial origin. In many cases, an incomplete EBV association is noted and confoundswhate role the virus plays in oncogenesis. A number of viral proteins have been shown to interact with epigenetic factors to regulate both viral and host gene expression. Thus, we hypothesize that EBV may inadvertantly induce epigenetic alterations to the host genome that are maintained upon loss of the virus. If proven, these results would broaden EBV's role in tumorigenesis and provide a mechanism for how a tumor virus can act in a "hit-and-run" fashion. We examined EBV-induced epigenetic alterations in a setting of viral redundancy and loss. With mounting evidence that EBV can induce epigenetic alterations, we developed a transient infection model where a clonal derivative (designated cl3) from the CCL185/A549 cell line was infected with a recombinant EBV carrying neomycin resistance cassette in place of the BDLF3 open reading frame. Infected cells were passaged ten times, and then selection pressure was removed for an additional ten passages to allow for viral loss. Three transiently-infected EBV-negative clones were identified by single cell cloning (designated 10-9, 10-10, and 10-14). Uninfected parental clone and cells transfected with pcDNA3 plasmid were passaged alongside the transiently-infected clones. Each sample was analyzed in duplicate.