Journal
NATURE GENETICS
Volume 52, Issue 12, Pages 1294-1302Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41588-020-00732-8
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Funding
- Common Fund of the Office of the Director of the National Institutes of Health
- NCI
- NHGRI
- NHLBI
- NIDA
- NIMH
- NINDS
- Wellcome Trust [102898/B/13/Z]
- Francis Crick Institute [FC001099, FC001206, FC001078]
- Cancer Research UK
- UK Medical Research Council
- MRC [MC_U117597139] Funding Source: UKRI
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Angiotensin-converting enzyme 2 (ACE2) is an entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and a regulator of several physiological processes.ACE2has recently been proposed to be interferon (IFN) inducible, suggesting that SARS-CoV-2 may exploit this phenomenon to enhance viral spread and questioning the efficacy of IFN treatment in coronavirus disease 2019. Using a recent de novo transcript assembly that captured previously unannotated transcripts, we describe a new isoform ofACE2, generated by co-option of intronic retroelements as promoter and alternative exon. The new transcript, termedMIRb-ACE2, exhibits specific expression patterns across the aerodigestive and gastrointestinal tracts and is highly responsive to IFN stimulation. In contrast, canonicalACE2expression is unresponsive to IFN stimulation. Moreover, theMIRb-ACE2translation product is a truncated, unstable ACE2 form, lacking domains required for SARS-CoV-2 binding and is therefore unlikely to contribute to or enhance viral infection. A truncated angiotensin-converting enzyme 2 (ACE2) isoform that lacks domains required for severe acute respiratory syndrome coronavirus 2 binding exhibits tissue-specific expression patterns and is responsive to interferon stimulation, in contrast to full-length ACE2, which is unresponsive to interferons.
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