Abstract
Se is a micronutrient essential for human health. Sub-optimal Se status is common, occurring in a significant proportion of the population across the world including parts of Europe and China. Human and animal studies have shown that Se status is a key determinant of the host response to viral infections. In this review, we address the question whether Se intake is a factor in determining the severity of response to coronavirus disease 2019 (COVID-19). Emphasis is placed on epidemiological and animal studies which suggest that Se affects host response to RNA viruses and on the molecular mechanisms by which Se and selenoproteins modulate the inter-linked redox homeostasis, stress response and inflammatory response. Together these studies indicate that Se status is an important factor in determining the host response to viral infections. Therefore, we conclude that Se status is likely to influence human response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and that Se status is one (of several) risk factors which may impact on the outcome of SARS-CoV-2 infection, particularly in populations where Se intake is sub-optimal or low. We suggest the use of appropriate markers to assess the Se status of COVID-19 patients and possible supplementation may be beneficial in limiting the severity of symptoms, especially in countries where Se status is regarded as sub-optimal.
Highlights
A link between Se deficiency and human disease was first demonstrated by the discovery in China that the aetiology of Keshan disease involved both coxsackievirus infection and a low intake of the micronutrient Se[1,2]
Fish and shellfish are relatively high in Se content but, for most foods, Se content is dependent on the level of Se present in the soil; this geographical variation is reflected in the Se status of different human populations, many of which have blood Se that is regarded as sub-optimal (≤85 μg/l)(5,6), for example, in parts of Europe including the UK
The COVID-19 pandemic raises three major questions in relation to Se: (i) to what extent does Se intake, sub-optimal intake as well as severe deficiency, affect responses to viral infection; (ii) what are the biochemical mechanisms supporting a role of Se in the host response and (iii) could Se intake be a factor in determining the response to COVID-19 infection? In this article, we address these questions by firstly reviewing the literature concerning the effects of Se on RNA virus infections, secondly by exploring how Se modulates the inter-linked redox homeostasis, stress response and inflammatory response mechanisms and by considering these effects in relation to recent observations on COVID-19
Summary
The first evidence that there might be a link between Se status and susceptibility of humans to a viral infection came from the study of Keshan disease, a myocardiopathy associated with heart failure and death, among the population in Heilongjiang province in China[1]. Two studies indicate that sub-optimal Se status lowers the number of CD4 T cells and increases both disease progression and death rates in HIV-infected patients[20,21]. No human studies have assessed the impact of Se status on the disease associated with West Nile virus, another RNA virus, in vitro infection of kidney epithelial cells leads to lower virus-induced cell death in Se-supplemented conditions[23]. This study supports animal work on IV and CVB showing that higher Se status enhanced the host response to a viral infection and promoted generation of mutations that increase virulence of RNA viruses, and provides evidence that similar effects occur in humans within a range of Se status found commonly in the UK population and worldwide. Dietary Se is converted in the body into the amino-acid selenocysteine which is incorporated into proteins, Dietary Se
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