The most pronounced interaction change, observed immediately upon infection, was the loss of SIRT3 association (by > 3 fold, not detected at 6, 24, 48, 96, and 120 hpi) with the acetyl-CoA acyltransferase 2 (ACAA2, also known as 3-Ketoacyl-CoA thiolase), a predicted substrate of SIRT3 (Fig 6B) [33,34,40]. This evidence concerns the gene ACAA2 and infection.