Research on the chemical mechanism and reciprocal behavior of the coronavirus relate to living organisms, engaging in the give and take of electrochemical mediators, is a very important, controversial and vital issue. What we should accept is the chemical identity of this scenario, and not preferably a characteristic of a biological system. This chemical reaction should be familiar, referring to the theory of chemical pathways involved in DNA/proteins in the body against aggressive guests (such as viruses). From the point of view of a chemist, this simple reaction is nothing more than an oxidation-reduction reaction (redox-stress signaling) which conducted and carried out by coronavirus in a biointerface medium. Thereby, oxidizing as well as reducing reagents should be very constructive, promoting development in such chemical process. We understand redox reactions as switchable thiol/disulfide exchanges (formation and cleavage of inherent disulfide bonds), then, we can hugely profit from redox-responsive nano-surfaces equipped with multiple new ionic and covalent interactions. This game-changing idea can substantiate by surface modified-nanoparticles to play powerful roles in synthesis of nano oxidizers as well as reducing agents in nanomedicine. Chemists and pharmacists must then explore new thoughts and present modern experiences/approaches of preparation nanoparticles and nanocomposites to create novel vaccines as well as coronavirus drugs. In this regard, this experience can also be so helpful for HIV/AIDS, which is caused by viruses.

Repair mechanisms following lung injury involve proliferation and migration of healthy epithelial cells in the vicinity of the injury to the site of injury. We have used a model of in vitro wound repair using monolayers of LA4 and A549 epithelial cell lines to study changes in the expression of molecules involved in cell-to-cell adhesion and migration during wound healing process. We have demonstrated that the poly-dispersed acid-functionalized-single-walled carbon nanotubes (AF-SWCNTs) block cell migration and cell division in this model and correlated this inhibition with molecular changes. Flow cytometric and confocal microscopy studies indicated that AF-SWCNTs were efficiently internalized by both cell lines. Examination of the wound repair process by live-cell imaging time-lapse micrography indicated that the active cell proliferation around the scratch wound area was completely blocked by AF-SWCNTs in LA4 cells and significantly inhibited in A549 cells. Assessment of cell migration across permeable membrane in trans-well cultures further indicated a marked inhibition of migration of both cells by AF-SWCNTs. Cellular expressions of proteins like β-catenin, NM-myosin, and vimentin having crucial roles in cell migration were suppressed by AF-SWCNTs whereas the expression levels of E-cadherin and Claudin-1, involved in cell-cell adhesion remained unaltered. Sustained cell to cell adhesion in presence of AF-SWCNTs prevents cells to detach and migrate. Our results indicate that AFSWCNT induced blockage of cell division and migration of epithelial cells and prevention of the detachment of cells from the monolayers needed for wound repair may be important factors responsible for suppression of wound repair process in monolayers of lung epithelial cells.