The way that SARS-CoV-2 virus enters the body and the state of the immune system itself are thought to be two primary differences in how children and adults become infected with coronavirus.
SARS-CoV-2 enters the body by binding to angiotensin converting enzyme-2 (ACE2), which is attached to the outer surface of cells in the lungs, arteries, heart and other organs. Studies have found that expression of ACE2 in the lungs increases with age. Infants and very young children have very low ACE2 expression, and older children have lower expression than adults. Research suggests that children may be protected from the serious respiratory components of COVID-19—including acute respiratory distress syndrome—due to their reduced ACE2 expression.
The immune system also plays a role in infection. Imbalance between mediators that increase versus suppress the inflammatory response plays a critical role in the clinical manifestations of this disease. Heightened immune response is often a factor in the inflammatory "cytokine storm" phase of COVID-19, in which the body attacks itself. Studies have shown that older mice had lower levels of the anti-inflammatory substances IL-10 and IL-13 and higher levels of pro-inflammatory chemicals in the lungs than younger animals.
CD4 T-cells, which play an important role in controlling viral replication and disease severity, are markedly decreased in adults with severe COVID-19.
In addition, lung tissue in children naturally has a higher concentration of regulator T-cells, which may protect against severe COVID-19 by suppressing the immune response that, in adults, may lead to uncontrolled inflammation.
