In this review, the relevance of selenium (Se) to viral disease will be discussed paying particular attention to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease (COVID-19). Se, the active centre in selenoproteins has an ongoing history of reducing the incidence and severity of viral infections. Host Se deficiency increased the virulence of RNA viruses such as influenza A and coxsackievirus B3, the latter of which is implicated in the development of Keshan disease in north-east China. Significant clinical benefits of Se supplementation have been demonstrated in HIV-1, in liver cancer linked to hepatitis B, and in Chinese patients with hantavirus that was successfully treated with oral sodium selenite. China is of particular interest because it has populations that have both the lowest and the highest Se status in the world. We found a significant association between COVID-19 cure rate and background Se status in Chinese cities; the cure rate continued to rise beyond the Se intake required to optimise selenoproteins, suggesting an additional mechanism. Se status was significantly higher in serum samples from surviving than non-surviving COVID-19 patients. As regards mechanism, SARS-CoV-2 may interfere with the human selenoprotein system; selenoproteins are important in scavenging reactive oxygen species, controlling immunity, reducing inflammation, ferroptosis and endoplasmic reticulum (ER) stress. We found that SARS-CoV-2 significantly suppressed mRNA expression of GPX4, of the ER selenoproteins, SELENOF, SELENOM, SELENOK and SELENOS and down-regulated TXNRD3. Based on the available data, both selenoproteins and redox-active Se species (mimicking ebselen, an inhibitor of the main SARS-CoV-2 protease that enables viral maturation within the host) could employ their separate mechanisms to attenuate virus-triggered oxidative stress, excessive inflammatory responses and immune-system dysfunction, thus improving the outcome of SARS-CoV-2 infection.

Chattopadhyay et al. [Biosystems (2003),68, pp. 5-17] proposed and analyzed an N – P model in the presenceof viral infection on phytoplankton population. They studied thedynamics under the constant nutrient input. The present paper dealswith the problem with seasonal variability on nutrient input. We usea general periodic function for nutrient input. We observe thedynamics of the system by considering (i) the infected phytoplanktonconsumes nutrient and (ii) the infected phytoplankton is not in astate to consume nutrient. Conditions for the persistence andextinction of populations are worked out. Our numerical experimentsshow that if the infected phytoplankton does not take nutrient thensusceptible phytoplankton coexists with the infected ones. But ifthe infected phytoplankton consumes nutrient then there is a chancefor extinction of susceptible phytoplankton for high rate ofinfection. We also observe that periodic nutrient input enforces thesystem to enter into chaotic region.