Abstract
Viral infections are a natural and inevitable part of life. In healthy individuals, mortality increases when the body’s innate immune system quickly activates, creating a cytokine storm. A rapid and excessive release of cytokines into the bloodstream can cause acute respiratory distress syndrome and death. This communication proposes inhibiting cytokine storm development through forced atopy. Hyper-allergenic skin cream therapy stimulates adaptive immunity to support innate immunity before acute infection.
Highlights
The human influenza A virus is a natural biological entity that spreads disease annually in the United States
Evidence suggests that the severity of COVID-19 is associated with an increased level of cytokines, and other inflammatory mediators, leading to acute respiratory distress syndrome [3]
In a communication published in the journal European Journal of Gastroenterology & Hepatology (2020) titled, “Eosinophilic esophagitis: is the Th2 inflammation protective against the severe form of COVID-19?” the researchers write, “Evidence could suggest that eosinophilic esophagitis and other allergic diseases, characterized by a Th2-skewed immunity, may be protective against severe COVID-19 disease and could support the hypothesis that eosinophils have a protective effect on SARS-CoV-2 infection” [12]
Summary
The human influenza A virus is a natural biological entity that spreads disease annually in the United States. It is the only influenza virus known to cause flu pandemics; its mutations can be highly infectious and spread quickly [1]. Evidence suggests that the severity of COVID-19 is associated with an increased level of cytokines, and other inflammatory mediators, leading to acute respiratory distress syndrome [3]. The innate immune system is the first line of defense against a new pathogen (e.g., mutated virus). It directs the qualitative and quantitative nature of adaptive immunity. Hyper-allergenic skin cream therapy inhibits cytokine storm development by stimulating adaptive immunity and increasing the efficacy of cytokine pleiotropy before acute infection
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