Vitamin D is a fat-soluble molecule synthesized from 7-dehydrocholesterol in the skin exposed to UVB radiation. Two forms are obtained by diet – colecaciferol and ergocalciferol. Vitamin D formed through skin synthesis undergoes 25-hydroxylation and 1-alpha-hydroxylation by CYP2R1 and CYP27B1 enzymes to be converted into metabolically active forms. Levels of minerals calcium and phosphorus and many hormones, mainly PTH and FGF23 affect vitamin D metabolism which is autoregulated as well. In plasma, vitamin D binding protein transports vitamin D and its metabolites. The elimination half-life varies depending on each metabolite affinity for DBP and takes place mostly through the bile. The excess is stored in adipose tissue. Vitamin D effects are mediated through binding to the intracellular VDR, which then forms a heterodimer with the RXR which binds to specific DNA sequences in the promoter region of the gene, the so-called response elements. Consequently, it affects the transcription of about two hundred target genes including the gene for its own receptor. Vitamin D regulates the metabolism of the minerals calcium and phosphorus, cell proliferation and differentiation including immunological and malignant cells. According to the EFDA, the desirable serum level of 25-OH-vitamin D is 50nmol/L in all age groups. The RDA for vitamin D counts 600 IU for adults, pregnant women and all children except 400 IU for children up to one year of age. Vitamin D deficiency occurs due to insufficient exposure to sunlight, low intake, reduced absorption or impaired metabolism. It clinically manifests as rickets, osteomalacia, or pathological fractures depending on the patients' age. Macrophages, dendritic cells, T lymphocytes, and B lymphocytes express the VDR on the surface. Vitamin D modulates the innate and acquired immune response to antigens, controls the extent of the inflammation, reduces the secretion of proinflammatory cytokines and immunoglobulins, stimulates the production and secretion of bactericidal proteins. Vitamin D deficiency is associated with reduced resistance to infections and autoimmunity. In a number of diseases of autoimmune etiology, vitamin D has shown potential as an adjuvant option to standard therapy. Adequate vitamin D levels act protectively regarding prevention of acute respiratory infections including SARS-CoV-2 infection. This effect is particularly noticeable in population with vitamin D deficiency and when supplementation is administered on a daily or weekly basis but not a bolus dose. The number of infected patients is higher during the colder part of the year and among people with darker complexion due to lower UVB absorption. The entry point of SARS-CoV-2 is ACE-2 at the cell surface. The virus compromises the function of ACE-2 resulting in excessive vasoconstriction, tissue and endothelial damage. Severe clinical forms of COVID are characterized by impaired regulation of the immune response and cytokine storm. The administration of vitamin D has been shown to be successful in lowering IL-6 levels associated with complications and poor disease outcome. Further research is needed to confirm and accurately assess the therapeutic effects of vitamin D in the treatment of COVID 19.