Abstract
Three main approaches are used to combat severe viral respiratory infections. The first is preemptive vaccination that blocks infection. Weakened or dead viral particles, as well as genetic constructs carrying viral proteins or information about them, are used as an antigen. However, the viral genome is very evolutionary labile and changes continuously. Second, chemical agents are used during infection and inhibit the function of a number of viral proteins. However, these drugs lose their effectiveness because the virus can rapidly acquire resistance to them. The third is the search for points in the host metabolism the effect on which would suppress the replication of the virus but would not have a significant effect on the metabolism of the host. Here, we consider the possibility of using the copper metabolic system as a target to reduce the severity of influenza infection. This is facilitated by the fact that, in mammals, copper status can be rapidly reduced by silver nanoparticles and restored after their cancellation.
Highlights
For the last 100 years, various aspects of human life have been negatively affected by viral respiratory infections caused by the influenza virus, the respiratory syncytial virus, coronaviruses, and rhinoviruses, etc
It can be speculated that the effect of AgNPs saves mice from severe complications caused by influenza A virus (IAV) infection in the same way as the prion protein [117]
These results provide evidence that AgNPs may have beneficial effects on the course of IAV
Summary
For the last 100 years, various aspects of human life have been negatively affected by viral respiratory infections caused by the influenza virus, the respiratory syncytial virus, coronaviruses, and rhinoviruses, etc. Rather than searching for pharmacological targets in the viral genome/proteins, they are located within the metabolic systems of the host cells themselves Targeting these systems has an indirect influence on viral replication, potentially protecting the organism from influenza infections irrespective of virus and any acquired resistance to currently used antiviral agents. The virus contains 40–50 unanchored polyubiquitin chains with free C-termini, which are recruited from the host cell during virion assembly and used for the release of vRNPs in the infection cycle [36,37]. Each replicated genomic negative-sense vRNA (a perfect copy of the negative-sense vRNA of the initial virus) [42] adopts a hairpin structure and binds the RNA polymerase complex at its 30 -50 double-strand stem, while NP proteins are associated with the RNA throughout its length. The viral NA cleaving sialic acid from the cell-surface glycoproteins and glycolipids actively participates in this process
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
