All died of COVID with standard vitamin D, 25% survived if 10X more vitamin D (mice)

Dietary Vitamin D Mitigates Coronavirus-Induced Lung Inflammation and Damage in Mice

Viruses . 2023 Dec 15;15(12):2434. doi: 10.3390/v15122434.

Gabriel Campolina-Silva 1 2 3, Ana Cláudia Dos Santos Pereira Andrade 1 2 3, Manoela Couto 1, Paloma G Bittencourt-Silva 4, Celso M Queiroz-Junior 1, Larisse de Souza B Lacerda 1, Ian de Meira Chaves 1, Leonardo C de Oliveira 2, Fernanda Martins Marim 5, Cleida A Oliveira 1, Glauber S F da Silva 4, Mauro Martins Teixeira 2, Vivian Vasconcelos Costa 1 2

Suspect many more mice would have survived if had used larger doses of Vitamin D and/or loading doses were given (like for humans)

The COVID-19 pandemic caused by the SARS-CoV-2 (β-CoV) betacoronavirus has posed a significant threat to global health. Despite the availability of vaccines, the virus continues to spread, and there is a need for alternative strategies to alleviate its impact. Vitamin D, a secosteroid hormone best known for its role in bone health, exhibits immunomodulatory effects in certain viral infections. Here, we have shown that bioactive vitamin D (calcitriol) limits in vitro replication of SARS-CoV-2 and murine coronaviruses MHV-3 and MHV-A59. Comparative studies involving wild-type mice intranasally infected with MHV-3, a model for studying β-CoV respiratory infections, confirmed the protective effect of vitamin D in vivo. Accordingly, mice fed a standard diet rapidly succumbed to MHV-3 infection, whereas those on a vitamin D-rich diet (10,000 IU of Vitamin D3/kg) displayed increased resistance to acute respiratory damage and systemic complications. Consistent with these findings, the vitamin D-supplemented group exhibited lower viral titers in their lungs and reduced levels of TNF, IL-6, IL-1β, and IFN-γ, alongside an enhanced type I interferon response. Altogether, our findings suggest vitamin D supplementation ameliorates β-CoV-triggered respiratory illness and systemic complications in mice, likely via modulation of the host's immune response to the virus.

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