An Overview Of Recent Studies Regarding The Sars-Cov2 and Vitamin D Levels
Özet
This review explores the relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and vitamin D levels. Emerging in late 2019, SARS-CoV-2 causes COVID-19 by binding to host ACE2 receptors, primarily presenting with respiratory symptoms and potential lung damage. Vitamin D, synthesized through sunlight exposure or dietary intake, acts as a critical immune modulator by regulating gene transcription through the vitamin D receptor (VDR). Globally, vitamin D deficiency (serum 25OHD <20 ng/mL) is widespread, including high rates documented in Turkey. Numerous original studies and meta-analyses suggest a strong correlation between vitamin D deficiency and increased susceptibility to SARS-CoV-2, higher risks of severe clinical outcomes, intensive care admissions, and elevated mortality. Mechanistically, vitamin D enhances innate cellular immune responses by increasing the expression of peptides such as defensins and cathelicidins, maintains immune homeostasis by modulating T-cell functions, and potentially protects against acute lung injury by regulating the renin-angiotensin system. While multiple clinical observations indicate that vitamin D supplementation significantly reduces inflammatory markers and improves recovery rates, conflicting evidence from certain randomized trials and meta-analyses reports no substantial reduction in infection or death rates, leaving the exact therapeutic benefits of supplementation a subject of ongoing clinical evaluation.
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