Reduced graphene oxide nanosheets decorated with ZnS and ZnS-Ag nanoparticles are successfully prepared via a facile one-step chemical approach consisting of reducing the metal precursors on a rGO surface. Prepared rGO-ZnS nanocomposite is employed as an adsorbent material against two model dyes: malachite green (MG) and ethyl violet (EV). The adsorptive behavior of the nanocomposite was tuned by monitoring some parameters, such as the time of contact between the dye and the adsorbent, and the adsorbent dose. Experimental data were also simulated with kinetic models to evaluate the adsorption behavior, and the results confirmed that the adsorption of both dyes followed a pseudo 2nd order kinetic mode. Moreover, the adsorbent was also regenerated in a suitable media for both dyes (HCl for MG and ethanol for EV), without any significant loss in removal efficiency. Ag doped rGO-ZnS nanocomposite was also utilized as a photocatalyst for the degradation of the selected organic contaminant, resorcinol. The complete degradation of the phenolic compound was achieved after 60 min with 200 mg of rGO-ZnS-Ag nanocomposite under natural sunlight irradiation. The photocatalytic activity was studied considering some parameters, such as the initial phenol concentration, the photocatalyst loading, and the pH of the solution. The degradation kinetics of resorcinol was carefully studied and found to follow a linear Langmuir–Hinshelwood model. An additional advantage of rGO-ZnS and rGO-ZnS-Ag nanocomposites was antibacterial activity against Gram-negative bacterium, E. coli, and the results confirmed the significant performance of the nanocomposites in destroying harmful pathogens.

The COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. The persistent effects of COVID-19 have become a subject of significant concern amongst the medical and scientific community. This article aims to explore the probability of a link between the COVID-19 infection and the risk of lung cancer development. First, this article reports that SARS-CoV-2 induces severe inflammatory response and cellular stress, potentially leading to tumorigenesis through common pathways between SARS-CoV-2 infection and cancer. These pathways include the JAK/STAT3 pathway which is activated after the initiation of cytokine storm following SARS-CoV-2 infection. This pathway is involved in cellular proliferation, differentiation, and immune homeostasis. The JAK/STAT3 pathway is also hyperactivated in lung cancer which serves as a link thereof. It predisposes patients to lung cancer through myriad molecular mechanisms such as DNA damage, genomic instability, and cell cycle dysregulation. Another probable pathway to tumorigenesis is based on the possibility of an oncogenic nature of SARS-CoV-2 through hijacking the p53 protein, leading to cell oxidative stress and interfering with the DNA repair mechanisms. Finally, this article highlights the overexpression of the SLC22A18 gene in lung cancer. This gene can be overexpressed by the ZEB1 transcription factor, which was found to be highly expressed during COVID-19 infection.