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Please note that the variants for which they looked were in the genes which produce early nuclear antigens. We already know that EBV has several latent states, and only one of these is completely inactive. Most latent EBV is still capable of producing early nuclear antigens, but stops short of producing proteins which lead to lytic replication.
Most medical thinking has been that the dangerous activity is confined to active, lytic replication which releases virions into the bloodstream. This is easy to detect because it causes cell death and significant antibody response. Early DNA replication inside a cell has been neglected because it is assumed to be incapable of transmission to other cells. The exception to this takes place when those cells are produced by clonal expansion of infected immune cells. Cells with multiple EBV episomes inside the nuclear membrane are capable of producing infected daughter cells via mitosis. If DNA replication inside these cells continues there is nothing to prevent a huge expansion in the number of infected immune cells. This is the normal way immune systems amplify a response to a tiny quantity of a particular antigen to produce a powerful immune response. If that response is being misdirected, serious pathology can result.
We have several problems here with standard medical thinking: 1) all EBV infecting people is not the same, it can even differ between physiological compartments in a single individual; 2) lytic replication is not the only dangerous activity; 3) genetic variants which change early nuclear antigens may escape detection entirely.
Early DNA replication inside a cell has been neglected because it is assumed to be incapable of transmission to other cells. The exception to this takes place when those cells are produced by clonal expansion of infected immune cells.