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Angiotensin-converting enzyme 2 inhibits lung injury induced by respiratory syncytial virus

Hongjing Gu1, Zhengde Xie2, Tieling Li3

  • 1State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, China.

Scientific Reports
|January 28, 2016
PubMed

Insights

Angiotensin-converting enzyme-2 (ACE2) protects against severe lung injury from respiratory syncytial virus (RSV) infection. ACE2 deficiency worsens RSV disease, but recombinant ACE2 protein offers therapeutic potential for RSV lung injury.

Area of Science:

  • Virology
  • Immunology
  • Pulmonology

Background:

  • Respiratory syncytial virus (RSV) causes severe lower respiratory illness in infants.
  • Mechanisms of RSV pathogenesis remain unclear.
  • No specific treatments exist for RSV infection.

Purpose of the Study:

  • Investigate the role of angiotensin-converting enzyme-2 (ACE2) in RSV-induced lung injury.
  • Explore ACE2 as a potential therapeutic target for RSV disease.

Main Methods:

  • Utilized an experimental mouse model of RSV infection.
  • Analyzed pediatric patient data.
  • Examined the role of the angiotensin II type 1 receptor (AT1R).
  • Administered recombinant ACE2 protein.

Main Results:

  • ACE2 protected against severe lung injury in RSV-infected mice and pediatric patients.
  • ACE2 deficiency exacerbated RSV-associated lung disease, mediated by AT1R.
  • Recombinant ACE2 protein treatment reduced the severity of RSV-induced lung injury.

Conclusions:

  • ACE2 plays a critical protective role in preventing RSV-induced lung injury.
  • ACE2 represents a promising therapeutic target for managing RSV lung disease.

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