Angiotensin-converting enzyme (ACE)2 receptor, an entry receptor for SARS-CoV and present on type 2 pneumocytes in the lung, ileal absorptive enterocytes, and nasal goblet secretory cells in nasal mucosa.
This paper shows, that ACE2 expression is upregulated by Type 1 IFNs. Furthermore it suggests that SARS-CoV-2 may use species-specific interferon up-regulation of ACE2, a mediator that protects tissues during lung damage, to increase infection. Hence type 1 IFNs, that drive anti-viral immunity on one hand, may paradoxically promote SARS-CoV-2 expansion by upregulating ACE2 expression on the other. As the type 1 IFN regulation in asthma might be impaired, these observations also might be related to the observed underrepresentation of severe Covid-19 among patients with asthma.

This article was selected by FJS van der Velden, MD (resident paeds) & G. Tramper, PhD, MD (paediatrician, paediatric infectiologist).