Thephysical clinical picture of both the acute disease and LC in younger children tendsto be less expressive and can be explained by physiological mechanisms such as thefunctioning thymus organ in children up to approximately 12 years of age, inaddition to the expressive deficiency of receptors of the biological catalyst thatconverts Angiotensin II (ACE2), vaccination status, and a significantly responsiveinnate immune system(17,28,33,34). This evidence concerns the gene AGT and laryngotracheoesophageal cleft.