Vitamin D deficiency and the course of SARS-CoV-2 infection

Abstract

Vitamin D is a fat-soluble steroid hormone. Its main role is to regulate calcium and phosphate levels, which are strictly associated with ossification and bone homeostasis. However, due to the presence of a nuclear vitamin D receptor (VDR) in the majority of cells of the human body, vitamin D also displays multiple effects beyond the bones. Calcitriol (1,25(OH)2D) not only affects cell growth and differentiation, but also stimulates the immune system by, for example, modulating the production of IL-4 and IL-5 anti-inflammatory cytokines. High numbers of VDRs have been found on macrophages, dendritic cells and lymphocytes, among other cells, which can be considered a very strong argument for the participation of vitamin D in autoimmune and anti-inflammatory processes. In recent months we have been witnessing the development of the COVID-19 pandemic. One of the most dangerous consequences of SARS-CoV-2 infection is acute respiratory distress syndrome caused by the activation of lung macrophages and the so-called cytokine storm. A recent study on COVID-19 patients suggests that vitamin D activates the innate immune response and suppresses the acquired immune response; the resultant decreased cytokine expression can reduce the severity of inflammation associated with COVID-19. Among older children and adults, vitamin D deficiency is widespread and observed worldwide, including in the Polish population. Based on numerous studies, normal serum vitamin D levels were established. Vitamin D concentration below 20 ng/mL is considered deficient and a level between 20 and 30 ng/mL is regarded as suboptimal. An optimal vitamin D concentration is 30–50 ng/mL.