Observations of increased AA in both acute SARS infection and in sera of high leak IBD patients (Table 1) signifies that AA has the potential to cross epithelial barriers into systemic circulation and inhibit the actions of DAAO, and thus has the capacity to be both a chemo-attractant to pathogenic opportunists (e.g., quinolone signal [25]) and the ability to limit DAAO H2O2 and myeloperoxidase (MPO) production in phagocytic cells, neutrophils and natural killer cells leading to long term evasion and viral dormancy within the host. This evidence concerns the gene MPO and inflammatory bowel disease.