Selenium and selenoproteins in viral infection with potential relevance to COVID-19

Zhang et al., Redox Biology, doi:10.1016/j.redox.2020.101715

Oct 2020

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Review of the role of selenium and selenoproteins in viral infections, with a focus on COVID-19. Authors present evidence that selenium deficiency is associated with higher COVID-19 mortality, and that higher selenium status correlates with higher cure rates in Chinese cities. Selenium supplementation has reduced severity and mortality for several other viral infections in past studies. Mechanistically, selenium may act through selenoproteins to reduce oxidative stress, moderate cytokine production, and support immune cell function. The main SARS-CoV-2 protease is inhibited by the synthetic selenium compound ebselen, suggesting redox-active selenium metabolites formed from high selenium intake could also potentially inhibit viral proteases. Authors propose selenium adequacy may prevent excessive inflammation in COVID-19, and that short-term supranutritional doses are unlikely to cause toxicity and may provide benefits in severe cases.

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Important missing comments or errors? Let us know.

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Zhang et al., 31 Oct 2020, peer-reviewed, 4 authors. Contact: m.rayman@surrey.ac.uk.

This Paper Selenium All

Selenium and selenoproteins in viral infection with potential relevance to COVID-19

Jinsong Zhang, Ramy Saad, Ethan Will Taylor, Margaret P Rayman

Redox Biology, doi:10.1016/j.redox.2020.101715

Selenium is a trace element essential to human health largely because of its incorporation into selenoproteins that have a wide range of protective functions. Selenium has an ongoing history of reducing the incidence and severity of various viral infections; for example, a German study found selenium status to be significantly higher in serum samples from surviving than non-surviving COVID-19 patients. Furthermore, a significant, positive, linear association was found between the cure rate of Chinese patients with COVID-19 and regional selenium status. Moreover, the cure rate continued to rise beyond the selenium intake required to optimise selenoproteins, suggesting that selenoproteins are probably not the whole story. Nonetheless, the significantly reduced expression of a number of selenoproteins, including those involved in controlling ER stress, along with increased expression of IL-6 in SARS-CoV-2 infected cells in culture suggests a potential link between reduced selenoprotein expression and COVID-19-associated inflammation. In this comprehensive review, we describe the history of selenium in viral infections and then go on to assess the potential benefits of adequate and even supra-nutritional selenium status. We discuss the indispensable function of the selenoproteins in coordinating a successful immune response and follow by reviewing cytokine excess, a key mediator of morbidity and mortality in COVID-19, and its relationship to selenium status. We comment on the fact that the synthetic redox-active selenium compound, ebselen, has been found experimentally to be a strong inhibitor of the main SARS-CoV-2 protease that enables viral maturation within the host. That finding suggests that redox-active selenium species formed at high selenium intake might hypothetically inhibit SARS-CoV-2 proteases. We consider the tactics that SARS-CoV-2 could employ to evade an adequate host response by interfering with the human selenoprotein system. Recognition of the myriad mechanisms by which selenium might potentially benefit COVID-19 patients provides a rationale for randomised, controlled trials of selenium supplementation in SARS-CoV-2 infection.

Authors' contributions All authors drafted sections of the manuscript. MPR prepared Table 1 and Fig. 1 . Figs. 2 and 3 were prepared by JZ. The online Supplemental file was prepared by MPR and JZ. All authors revised the manuscript to produce the final version. Declaration of competing interest None of the authors has any conflict of interests. Appendix A. Supplementary data Supplementary data to this article can be found online at https://doi. org/10.1016/j.redox.2020.101715 .

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