Vitamin D and SARS‐CoV‐2

The single‐stranded RNA virus, SARS‐CoV‐2, causing the COVID‐19 pandemic, has severely impacted daily life globally. It has been suggested to supplement the general population with vitamin D to reduce the impact of COVID‐19. Nevertheless, no clear consensus can be found as to whether vitamin D affec...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Basic & clinical pharmacology & toxicology 2023-07, Vol.133 (1), p.6-15
Hauptverfasser: Feentved Ødum, Sofie‐Louise, Kongsbak‐Wismann, Martin
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The single‐stranded RNA virus, SARS‐CoV‐2, causing the COVID‐19 pandemic, has severely impacted daily life globally. It has been suggested to supplement the general population with vitamin D to reduce the impact of COVID‐19. Nevertheless, no clear consensus can be found as to whether vitamin D affects COVID‐19 disease burden. Some studies found that vitamin D levels and/or vitamin D supplementation alleviated COVID‐19 disease severity and mortality. Contrarily, other studies found no such effects of vitamin D. To understand this lack of consensus, it is relevant to investigate molecular studies of the vitamin D receptor (VDR), as such studies might explain apparent controversies. We have investigated recent studies of how transcriptional regulation by the VDR affects the immune response against SARS‐CoV‐2. One study found that cells from severe COVID‐19 patients displayed a dysregulated vitamin D response. Contrarily, another study observed a normal immune response towards SARS‐CoV‐2 in a patient with a non‐functional VDR. These observations indicate that hypovitaminosis D is not a prerequisite for an efficient immune response against SARS‐CoV‐2 and therefore not a driving factor for developing severe COVID‐19. However, should a patient develop severe COVID‐19, vitamin D seems to be beneficial potentially by dampening the cytokine storm.
ISSN:1742-7835
1742-7843
DOI:10.1111/bcpt.13872