I'm trying to understand this plosone paper. I think Alices post above from the Ohio State University source is very helpful. Thanks for that Alice. So, my understanding is that there are two forms of virual replication. lysogenic, where the virus's nucleic acid integrates with the human DNA in the cell, and then when the cell replicates as normal it also unwittingly replicates the viral nucleic acid as well. The virus then presumably kills the cell. At any rate, the plos paper is talking about the other type of viral replication - Lytic - in which the virus having invaded the human cell, uses the host cell's mechanics and energy to replicate itself until the host cell bursts. The cell is dead and there are loads more virons on the lose ready to infect the next cell. The lytic cycle is quicker. A thought - what is causeing the Lytic replication to abort in the first place? They only found antibodies to these EBV encoded dUTPase and DNA polymerase proteins in 6 people originally, I they were treated with Valtrex. Then they talk about larger numbers being positive to antibodies for dUTPase (23/52 - 44.2%) and to the EBV DNA encoded polymerase (41/52 - 78.8%). Is this when they looked back at older samples they had taken? This finding looks really important to me the more I look at it. But it's important to understand whether this subset is 6/142 or the higher figure (23/52 for the first antibody and 41/52 for the second) Big difference. Can anyone work out which it is we're talking about?