Angiotensin-converting enzyme 2 (ACE2) serves as a functional receptor to SARS-CoV.13 , 14 SARS-CoV also disrupts the urokinase pathway, which controls fibrin levels through extracellular remodeling, and is associated with pulmonary hemorrhage and fibrosis.15 SARS-CoV also triggers the production of high levels of proinflammatory cytokines contributing to excessive inflammation in the lungs. Hence, anticytokine and chemokine immunotherapy may be effective for minimizing collateral damage.12