![]() ![]() Prophylactic administration of high-dose vitamin D 3 increased the expression of IFNB and reduced inflammation in the lungs after SARS-CoV-2 infection, although this was not associated with a survival benefit 2. Second, a study in transgenic mice expressing human ACE2 has shown that SARS-CoV-2 induces the expression of CYP27B1, which encodes the 1α-hydroxylase enzyme that catalyses the conversion of the major circulating metabolite 25-hydroxyvitamin D (25(OH)D) to 1,25(OH) 2D (ref. First, the vitamin D-inducible antimicrobial peptide cathelicidin LL-37 has been shown to inhibit SARS-CoV-2 attachment to host cells by blocking both the receptor-binding domain of the S1 subunit of the viral spike protein and the ligand-binding domain of the host-expressed viral entry receptor ACE2 (ref. The relevance of these actions for the host response to SARS-CoV-2 is supported by two lines of evidence. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH) 2D), induces innate antiviral effector mechanisms and regulates inflammation in response to infection with rhinovirus, respiratory syncytial virus and influenza viruses (Fig. ![]() The primary source is via cutaneous synthesis in response to sunlight, but it can also be ingested in the diet. Vitamin D belongs to a group of fat-soluble vitamins with vitamin D 3 being the major form in humans. ![]()
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