In contrast, the transient increase in EBNA2 binding to CD21, IL7 and HES1 in EBNA-LP-deficient infections (Fig 8B and 8C) followed by a transient surge in their transcript levels (Fig 6B–6D), could be explained by a direct relationship between EBNA2 and EBNA-LP, but one where EBNA-LP restrains or modulates the transactivation of those genes, rather than enhances it. Here, HES1 is linked to infection.