A novel isoform ofACE2is expressed in human nasal and bronchial respiratory epithelia and is upregulated in response to RNA respiratory virus infection

  1. Cornelia Blume
  2. Claire L Jackson
  3. Cosma Mirella Spalluto
  4. Jelmer Legebeke
  5. Liliya Nazlamova
  6. Franco Conforti
  7. Jeanne-Marie Perotin-Collard
  8. Martin Frank
  9. Max Crispin
  10. Janice Coles
  11. James Thompson
  12. Robert A Ridley
  13. Lareb S N Dean
  14. Matthew Loxham
  15. Adnan Azim
  16. Kamran Tariq
  17. David Johnston
  18. Paul J Skipp
  19. Ratko Djukanovic
  20. Diana Baralle
  21. Chris McCormick
  22. Donna E Davies
  23. Jane S Lucas
  24. Gabrielle Wheway
  25. Vito Mennella
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Abstract

Angiotensin-converting enzyme 2 (ACE2) is the main entry point in the airways for SARS-CoV-2. ACE2 binding to SARS-CoV-2 protein Spike triggers viral fusion with the cell membrane, resulting in viral RNA genome delivery into the host. Despite ACE2’s critical role in SARS-CoV-2 infection, an understanding of ACE2 expression, including in response to viral infection, remains unclear.

Until nowACE2was thought to encode five transcripts and one 805 amino acid protein. Here we identify a novel short isoform of ACE2. ShortACE2is expressed in the airway epithelium, the main site of SARS-CoV-2 infection; it is substantially upregulated in response to interferon stimulation and RV infection, but not in response to SARS-CoV-2 infection, and it shows differential regulation in asthma patients. This short isoform lacks SARS-CoV-2 spike glycoprotein high-affinity binding sites and altogether, our data are consistent with a model where shortACE2may influence host susceptibility to SARS-CoV-2 infection.

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