Brief Report: Vitamin D deficiency in SARS-CoV-2-induced ARDS

The SARS-CoV-2 virus has been an ongoing focus of research due to the severity of the pandemic on susceptible populations including older people. The inflammatory nature of SARS-CoV-2 infection suggests a dysregulated immune response as a primary component of pathogenicity and progression to acute respiratory distress syndrome (ARDS). Vitamin D levels are inversely associated with both clinically apparent upper respiratory viral syndromes as well as ARDS due to its effects in modulating the immune response. Vitamin D has been established as tempering inflammation by promoting T regulatory cell activity, increasing IL-10 release, and inhibition of interleukin-6 (IL-6) release from inflammatory cell subsets. Older populations show an age-related decline in Vitamin D levels, suggesting a susceptibility to deficiency and thus worse outcomes with infectious diseases that trigger inflammatory cytokine cascades such as SARS-CoV-2. Although not the only component, Vitamin D may be a safe and effective avenue in improving the morbidity of SARS-CoV-2 infection. Here, we evaluate the literature that Vitamin D deficiency plays a role as an independent risk factors in the pathogenesis of ARDS in SARS-CoV-2 patients through the disinhibition of IL-6 and the shift towards an inflammatory Th17 cell phenotype. The robust evidence within the literature prompt us to recommend monitoring of Vitamin D levels and sufficient Vitamin D supplementation in older patients before potential infection with SARS-CoV-2 to mitigate the development of severe symptoms including ARDS.