Table 1.
Rationale for potential preventive (Pr) and/or therapeutic (Th) use of selenium (Se) in COVID-19.
| References | Main points | Potential Se application in COVID-19 |
|---|---|---|
| RNA virus | ||
| (6, 8–11) | Se deficiency increases mutation, replication, and virulence of RNA viruses | As Pr in asymptomatic and Th in clinical settings for antiviral defense |
| (9, 30–32, 53, 54) | RNA viruses, including the SARS coronaviruses, likely divert cellular Selenium for their own selenoproteins and knockdown host TrxR/GPx (bioinformatic studies) | |
| (13) | Se supplementation decrease Keshan disease (linked to Coxsackie virus) prevalence | |
| (15, 16) | Se treatment reduced mortality Hantavirus infection (HFRS) in mice and humans | |
| (23–26) | Se supplementation HIV reduces disease progression and mortality | |
| (28, 29) | Se deficiency in population and patient-based studies associated with low recovery rate and mortality of COVID-19 | |
| Se general action | ||
| (86) | In vitro Se attenuates pro-inflammatory gene expression in macrophages | As Pr and Th of COVID-19 thrombosis and/or endothelitis and/or inflammatory complications |
| (57, 59) | In vivo Se supplementation increases platelet GPx activity and reduces aggregation through TXA2 inhibition and increased bleeding time | |
| (61, 62) | Se protects endothelial cells from oxidative insult | |
| (63) | In vitro, Se supplementation protects human endothelial cells from oxidative damage through TrxR and GPx induction | |
| (36, 45, 47) | Se mediates inhibition of the activation of the transcription factor NF-kB which regulates genes that encode inflammatory cytokines |
Se (Th) might modulate NFκB activation in SARS-Cov-2 (cytokine storm) |
| (44) | in animal study, Se Inhibition of Nf-kB in SARS-Cov infected mice increased survival | |
| (35) | Se inhibits the production of ROS in H1N1 infected cell models |
ROS effects, apoptosis oxidative stress (Th) |
| (36) | Se addition in cell media deficient in Se, counteracts ROS damages via GPx activity restoration | |
| Obesity, elderly | ||
| (81) | Obesity related oxidative stress has deleterious impact on cardiovascular disease (Framingham study) | Obesity and elderly as independent risk factor of severe COVID-19 |
| (80) | Obese hosts exhibit delayed and blunted antiviral responses to influenza virus infection | In both Pr, Th for complications: cardiovascular, endotheliitis, thrombosis, and to mitigate cytokine storm |
| (87) | In Bioinformatic study, Se deficiency alters miRNAs (miR-185-5p) that regulate selenoproteins expression (GPx) in oxidative stress and obesity | |
| (88, 89) | Obesity is tied to reduction of GPx3 activity in adipose tissue | In elderly, Se Pr as in asymptomatic and Th as soon as possible |
| In animal study, Selenite treatment increases GPx3 activity in obese mice | ||
| (96) | Serum Se level is significantly reduced among morbidly obese | |
| (106) | ex vivo study, Oxidative stress is highly increased in senescent fibroblasts that consume more Se. The addition of Se in these cells, increases GPx activity and decreases ROS | |
| (107, 110, 112) | In clinical study, In elderly subjects, the more Se deficiency the higher the mortality rate | |
| In RCT, Se supplementation in elderly reduces viral events and cardiovascular mortality | ||