Abstract
Modern epidemics quickly spread across borders and continents with devastating effects on both human health and the world economy. This issue is made worse by the various ways that infections are spread, including through aerosol, droplets, and fomites. The antibacterial qualities of various surface materials and coatings have been the subject of much research. However, the antiviral activity of metal coatings can be heavily influenced by imbalances in metal distribution and the presence of other metal impurities. As such, there is interest in developing novel surface coatings that can reduce the transmission of active viral particles in healthcare facilities. In recent years, the non-metals, such as selenium and nanoparticles, have acquired greater interest from the medical and scientific community for their antiviral surface activity. In this review, we will discuss the cellular and physiological functions of selenium in mammalian cells and against viral infections. We then discuss the mechanism behind selenium coated surfaces and their efficacy against bacterial infections. Lastly, we examine the antiviral activity of selenium, and the potential antiviral activity of selenium nanoparticles and coatings.
1. Introduction
Modern pandemics have been a persistent problem throughout human history leading to disruptions to human health and the world economy. In recent years, this issue has worsened with the emergence of contagious infections that spread through several methods including, through aerosol, droplets, and fomites. Historically, the usual method for reducing the spread of bacterial and viral pathogens has included multiple-barrier protection (e.g., personal protective equipment), strict hygiene standards, and immunization programs [1]. The antibacterial qualities of various surface materials and coatings have been the subject of much research. Many surface materials have both antiviral and antimicrobial capabilities. Some of the novel surface coating methods to reduce viral particle transmission have included passive pathogen-repellent surfaces, surface-bound active antimicrobials, and biocidal coatings. One common surface coating method includes metal coated surfaces, such as silver, gold, and cobalt [2,3]. However, the antiviral activity of metal coatings can be heavily influenced by imbalances in metal distribution and the presence of other metal impurities. Furthermore, there are significant variations in how different bacteria and viruses react to different prophylactic and therapeutic methods [1]. As such, there is interest in developing novel surface coatings and novel antiviral substances, such as nanoparticles, that can reduce the transmission of active/infective viral particles [4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19].
In recent years, the non-metals, such as selenium, have acquired greater interest from the medical and scientific community for their antiviral activity using nanoparticles or selenium coated surfaces [19,20]. Due to their unique physical and chemical properties, nanoparticles have been the subject of extensive research over the past few decades. Nanomaterials’ primary characteristics are mostly determined by their shape and particle size, which is between 1 and 100 nanometers (nm) in diameter [19,20]. Given that selenium (Se) is an essential element with numerous functions in the human body, including protection of the cardiovascular and liver organs, selenium nanoparticles (SeNPs) have attracted significant interest for their unique properties to treat several different disease processes [19,21,22,23]. In this review, we will discuss the cellular and physiological functions of selenium in mammalian cells and against viral infections. We then discuss the mechanism behind selenium coated surfaces and their efficacy against bacterial infections. Lastly, we examine the antiviral activity of selenium, and the potential antiviral activity of selenium nanoparticles and coatings.
2. Physiological Functions of Selenium
Inorganic minerals, such as selenide, selenate, and selenite, are abundantly dispersed in the crust of the Earth [24]. Virtually all living things require selenium for optimum health [25]. Selenium is found in biological systems in the forms of selenocysteine, dimethyl selenide, selenomethionine, and selenomethylcysteine [26,27,28,29]. These diverse forms of selenium are integrated as selenocysteine in enzymes used to control several biological functions, such as the immune system response and thyroid function [29,30,31]. In particular, selenoproteins are important components of the cellular antioxidant machinery, which scavenge free oxygen radicals to protect tissue against oxidative damage [32,33]. Among the 25 discovered human selenoproteins, glutathione peroxidase has gained widespread acclaim for catalyzing the oxidation of monomeric glutathione into glutathione disulfide and the reduction of hydrogen peroxide into water by using selenocysteine as a prosthetic group [34,35].
In addition to its antioxidant activity, recent studies examining selenium have shown its importance in preventing the spread of viral infections within the body. The majority of selenium’s health benefits result from the incorporation of selenocysteine into selenoproteins [36]. The UGA codon, which is often used as a signal to stop protein synthesis, is used to encode selenocysteine. Specifically, a selenium atom substitutes a sulfur atom in the structure and function of selenocysteine, giving it increased catalytic activity [36]. The following sub-families of selenoproteins have been thoroughly characterized: glutathione peroxidase, thioredoxin reductases, methionine sulfoxide reductase, and selenoproteins in the endoplasmic reticulum. Selenoproteins are essential for many molecular pathways, including those involving oxidative stress response, redox regulation, mitochondrial function, endoplasmic reticulum stress, and immune and inflammatory responses against viral infections [37]. Cross-talk between these pathways are crucial to produce a sufficient response to viral infections [37]. In addition, sufficient selenium in the body also maintains the structural and functional integrity of pulmonary epithelial barriers since selenoproteins reduce lipid and phospholipid hydroperoxides to protect epithelial barriers from reactive oxygen species (ROS) [37]. Similarly, antioxidant selenoproteins shield neutrophils from inward oxidative stress. As such, it is not surprising that low selenium levels has been associated with a worse response to viral infections.
3. Selenium Deficiency and Viral Infections
Viruses with an affinity for the respiratory tract, such as the influenza virus, adenovirus, and respiratory syncytial virus cause a wide range of symptoms in patients, including nasal congestion, sore throat, fever, and severe acute respiratory distress syndrome [38]. When an individual is infected with a virus, the viral particle effects the body’s oxidant state, disrupting the equilibrium between prooxidants and antioxidants. Specifically, viruses cause the production of reactive oxygen species (ROS)-producing enzymes, such as xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate oxidases (NADPH oxidases, Nox), to decrease. This reduces the reduction capacity of the cell, leading to irreversible cell and tissue death [38]. This rise in ROS and consequent oxidative stress from viral infections create an environment that is conducive for viral replication [39]. Superoxide dismutase, catalase, peroxiredoxins, and glutathione peroxidases are antioxidant enzymes that play a significant part in reducing the oxidative stress secondary to viral infections [40]. Activation of inflammatory pathways results in an increase in cytokine production and consequent tissue damage after an increase in ROS from viral infections. The nuclear factor κB (NF-κB) signaling is activated by the elevated ROS during viral infections, which increases the buildup of inflammatory cytokines. These inflammatory cytokines are produced in excess, leading to a cytokine storm that severely damages major organs in the body, such as the lungs [41].
Tas, using murine in vivo studies, found that selenium deficiency decreased glutathione peroxidase activity and facilitated the emergence of viral variants with greater pathogenicity in patients carrying the human immunodeficiency virus (HIV) [42]. It is hypothesized that increased oxidative stress, brought on by the lack of glutathione peroxidase, causes a higher severity of viral infections in selenium-deficient hosts [29]. When compared to infected persons with adequate selenium levels, hospitalized HIV-infected patients with low selenium levels have a higher mortality rate. Additionally, selenium supplementation increased glutathione peroxidase activity and, subsequently, reduced HIV-1 activation [43]. In addition, a deficiency in selenium is associated with worsening progression and pathogenesis of several other viruses, including coxsackie virus, influenza, hepatitis B and C, poliovirus, and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) [44]. Overall, the importance of selenium against a wide range of viral infections makes selenium an attractive for antiviral coatings given its versatility and low cost. In the subsequent sections, we propose a mechanism by which selenium coatings eliminate viral particles and current studies showing their effectiveness.
7. Conclusions
Selenium coatings remain an attractive method for reducing the spread of bacteria and viruses. There is a wide range of substances with antiviral and antibacterial activities. There are several alternatives when novel chemistries are designed and engineered, which is another possibility. These materials’ antimicrobial characteristics have received a lot of attention, but there are much less data on their antiviral activities, which is a gap that needs to be filled. It is obvious that material science may contribute significantly to the creation of theoretical and actual strategies to contain infectious outbreaks. It is important to consider both tried-and-true and novel broad-spectrum antiviral tactics because they might help us better prepare for and face the challenge of upcoming viral pandemics.
Author Contributions
Conception and design: J.K., J.F. and T.W.R. Manuscript writing: J.K., J.F. and T.W.R. Final approval of manuscript: T.W.R. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
Not applicable.
Informed Consent Statement
Not applicable.
Data Availability Statement
Not applicable.
Conflicts of Interest
The authors declare no conflict of interest.
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