Antiviral Activities of Cu2+ Ions in Viral Prevention, Replication, RNA Degradation, and for Antiviral Efficacies of Lytic Virus, ROS-Mediated Virus, Copper Chelation

Copper has been known for decades that marked changes of micronutrient homeostasis in the host are accompanied by infection or inflammation. Copper levels in the serum are significantly elevated in response to inflammation that copper accumulates at sites of inflammation. Easily oxidized copper oxide nanoparticles (CuONPs) are widely used as catalysts that the ability of CuONPs to reduce bacterial population and virus application is enhanced. The mechanism of copper-mediated inactivation of herpes simplex virus (HSV) is by which cupric ions oxidatively damage biomolecules. Virus-mediated subjugation and modulation of host lipids during infection that the life cycle of most viruses proceeds through a series of basic steps: binding and internalization, fusion, uncoating, of the viral genome, its replication, assembly of new particles, and budding or release of the newly made viruses. The HIV-1 protein Vpu is an 81-amino-acid (16-kDa) type I which the presence of Vpu leads to the degradation of BST-2 via an endosome-lysosome degradation pathway. Oxidative degradation by a Cu-metalloenzyme, and ubiquitin-mediated degradation of cellular proteins were exploited. Copper can disrupt the lytic cycle of the Coccolithovirus. Lysins represent a novel class of anti-infectives derived from bacteriophage which lysins are bacterial cell wall hydrolytic enzymes that selectively and rapidly kill specific bacteria. Regarding copper induced cellular toxicity, several mechanisms have been proposed based on the formations of ROS by free Cu ions as cupric and cuprous ions can participate in redox reactions. ROS (O2ˉ,･OH, OHˉ), Cu+ and H2O2 play the important roles for viral inactivations. Thujaplicin-copper chelates inhibit influenza virus-induced apoptosis. Pyrrolidine dithiocarbamate as a metal ion binding agent inhibits the activity of the viral proteases of polyprotein processing and RNA replication of HRV. Chelation enables metals are capable of ligand scavenging via complexation, since reverse transcriptase enzyme inhibits the growth and replication of RNA tumor viruses. Thus, copper complex and copper chelation enhance antiviral efficacy.