Intestinal barrier disruption during SARS-CoV-2 infection might be explained by several mechanisms: a direct viral infection of intestinal epithelial cells (238); down-regulation of ACE2 after viral infection of enterocytes (239); systemic inflammation sustained by cytokine storm (226); IL-6-mediated vascular damage (240); intestinal inflammation sustained by gut homing of T cells, as suggested by high plasma levels of CCL25, a gut homing marker, ligand for the chemokine receptor CCR9 (234, 241), and gut dysbiosis with subsequent mucosal inflammation (226, 242). This evidence concerns the gene CCL25 and viral infectious disease.