PATHOGENESIS

• Virus attach to a host cell receptor (the angiotensin-converting enzyme 2 (ACE2)

receptor), by the help of the spike (S) protein of the virus.
• SARS-CoV-2 reduces expression of ACE2 in lung cells, and loss of pulmonary ACE2
function causing acute lung injury.
• ACE2 also regulates the renin-angiotensin system (RAS), causing reduced ACE2
function
• influences blood pressure,
• fluid and electrolyte balance, and enhances inflammation
• and vascular permeability in the airways.
• The binding of the virus to the ACE2 receptor triggers
• Endocytosis of the virion,
• Replication
• Assembly,
• Maturation, and
• Release

• Local immune response, recruit

• macrophages and monocytes that respond to infection,
• release cytokines, and prime adaptive T and B cell immune responses.
In a case of Dysfunctional immune response it can cause severe lung and even
systemic pathology.
Pyroptosis is a highly inflammatory form of programmed cell death which is
capable of inducing death and injury of virus-infected cells and tissues.
Cytokine storm that mediates widespread lung inflammation as well as systemic
manifestations such as
Multiorgan failure,
Septic shock, and
Myocardial damage with circulatory failure.
Most children and adolescents present with mild to moderate symptoms, mortality
rate in children was reported to be at 0.09%
Theories regarding the severity and
susceptibility of children to COVID-19
• ACE2 Receptor
• Role of other viruses
• Reduces exposures
• Aging of the immune system
• Innate vs adaptive immune system
• Inflammation
e ACEACE2 receptor is expressed in airway epithelial cells, a