ACE2 deficiency significantly worsened disease pathogenesis and survival in H7N9-infected mice, resulting in 0% survival compared to 20% in wild-type mice.
Does ACE2 deficiency worsen acute lung injury in an experimental mouse model of influenza A (H7N9) virus infection?
ACE2 plays a critical protective role in H7N9-induced acute lung injury, suggesting it as a potential therapeutic target.
Absolute Event Rate: 0% vs 20%
Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks.
Yang et al. (Thu,) conducted a other in Influenza A (H7N9) virus-induced acute lung injury. ACE2 deficiency vs. Wild-type was evaluated on Survival rate. ACE2 deficiency significantly worsened disease pathogenesis and survival in H7N9-infected mice, resulting in 0% survival compared to 20% in wild-type mice.