Next, to identify immune mechanisms facilitating control of escape virus in minority of rats, we compared intrahepatic T cell responses between infection outcome groups (resolvers vs. non-resolvers) at day 84–91 p.i. No significant difference was found in the frequency of cytokine-producing CD8 T cells specific for the escape-prone NS3974 or NS4A1578 epitopes that were mutated in escape virus; responses against the E1191 epitope were absent in both groups (Fig 5A), possibly to due to failed priming by variant peptide. Here, CD8A is linked to infection.