The integration of these temporal SIRT3 interactions with measurements of protein abundance, acetylation, and viral titers led us to propose a model (Fig 6H) where HCMV infection disturbs the SIRT3-ACAA2 association, resulting in hyper-acetylation and inhibition of ACAA2, an inhibition that functions to support viral replication. Here, ACAA2 is linked to cytomegalovirus infection.