Fig. 1: Vitamin D in viral infection.
Vitamin D from cutaneous synthesis or oral intake is converted in the liver to 25-hydroxyvitamin D (25(OH)D), the major circulating vitamin D metabolite. In pulmonary epithelium and in leukocytes, respiratory viruses induce the expression of the 25(OH)D hydroxylase CYP27B1, which converts 25(OH)D to the active vitamin D metabolite 1,25-dihydroxyvitamin D (1,25(OH)2D). This supports antiviral effector mechanisms and regulates inflammation by reducing TNF expression, increasing the ACE2:ACE ratio, inhibiting the development of TH1 and TH17 cells, and promoting the development of Treg cells. These anti-inflammatory actions may reduce disease severity associated with cytokine storms. CYP24A1 can catabolize 25(OH)D to the relatively inactive metabolite 24R,25-dihydroxyvitamin D (24R,25(OH)2D).
