La revue de presse / The press review
Covid-19 is a multi-factorial disease. When symptoms appear, virus is already growing in the nasal mucosa cells, newly generated free virus particles are already poring on the nasal mucosa, immune system is trying hard to control the infection by releasing multiple disease related cytokines (IL-6, TSLP, IL-2, IL-4) on infected surfaces, severe inflammation is already installed in nasal mucosa and progressing towards upper respiratory tract (URT), and systemic immune & inflammatory cascades are already installed.
The only way to stop disease progression is therefore to stop virus growth and its dissemination in other organs such as lungs to stop cellular destruction and consequently the inflammatory cascade.
A specific antiviral drug, acting topically, and capable to block virus growth in nasal cavity and URT would be an ideal approach to avoid side effects but such topical antivirals are not yet available. Using anti-inflammatory drugs would be another alternative but it may not totally suppress the disease as virus would continue destroying cells and triggering immune reaction. Current results with such drugs to treat Covid-19 infection have not shown encouraging results. Repairing damaged nasal mucosa to stop free virus &/or cytokine systemic entry may also help minimize inflammatory cascade by reducing free virus particle or cytokine systemic entry but there are no cell growth stimulating treatments. This is because cell growth needs an infection and chemical free environment which cannot be achieved if virus continue growing, if cells are inflamed, and if nasal surface contains multiple pro-inflammatory cytokines.
The combination of these factors leads to excessive stress on the immune system which gets exhausted and in certain cases, as a last attempt to supress the infection, release suddenly a huge quantity of cytokine (IL-6 & others), called as cytokine release syndrome (CRS). Widespread inflammation of URT leads to the exudation of liquid in the lungs and finally drowning of the lungs due to respiratory failure.
Taking into consideration the complexity of the disease involving viral growth, nasal mucosa damage, free systemic passage of virus and cytokines into the circulation maintaining inflammatory cascade, immune exhaustion, and widespread lung inflammation leading to respiratory distress, no single drug or medical device can act simultaneously on all these parameters. Once the Covid-19 symptoms appear, only a multi-target approach should help minimize the chances of occurring of CRS.
COVISPRAY MEDICAL DEVICE:
Covispray is a filmogen liquid containing glycerol, two jellifying agents, and an association of plant polymers, all capable to bind with glycerol molecules to render it filmogen, flexible, and resistant to mechanical pressures exerted by the liquid flow. When applied in the nasal cavity, the liquid forms a transparent and slightly osmotic film, like a liquid barrier, on the nasal surface. The thickening / jellifying agents in the film swells when they meet water and renders the film absorbent.
This film can capture all environmental pollutants entering the nasal cavity. Being osmotic, the film attracts hypotonic liquid from the inner parts of the nasal mucosa thereby detaching and draining all the contaminants present on the surface of the nasal mucosa which are then trapped in the filmogen liquid.
A few H-OH binding sites of all the polymeric ingredients in the film binds with glycerol but as the polymers are known to have strong affinity for specific proteins, and as the Covid-19 RBD and virus S spikes are proteins, the remaining free polymer binding sites may bind and trap the virus particles. Trapped virus particles become inactive and cannot infect new healthy cells.
The nasal surface inflammatory cytokines are attracted osmotically by the Covispray film which helps minimizing their concentration on the nasal surface.
A few Covispray polymers equally binds to cytokine protenis such as IL-6 and TNF-alpha. Neutralizing these pro-inflammatory cytokines help minimize immune stress and consequently the chances of immune burn-out.
Other free-floating contaminants on the nasal mucosa are also attracted osmotically towards the film and are captured. This mode of action helps cleaning the nasal mucosa through mechanical effects without being in contact the with live, damaged nasal cells.
Repairing the cellular damage and injuries is a natural physiological function of the body and starts as soon as there is a breach of cellular integrity. Damaged nasal mucosa cannot repair easily because of continuing viral growth, inflammation, and the presence of a huge concentrations of multiple pro-inflammatory cytokines on the surface. When nasal surface is cleaned osmotically and most of the virus particles are trapped in the absorbent film, inflammation starts reducing immediately, offering ideal conditions for cell growth and natural healing. An intact and healthy nasal mucosa defend itself against infection and forms a tight barrier against incoming pathogens. Minimizing or stopping free entry of pathogens into the systemic circulation should help supress inflammatory cascade and pressure on the immune system.
The aim of Covispray is not to act as an antiviral or anti-cytokine drug but just to minimize the concentration of pathogen and the risk factors which continue triggering and maintaining inflammatory cascade. Minimizing immune load should help immune system work normally to defend the body and to avoid occurrence of CRS.