Cigarette smoke exposure and inflammatory signaling increase
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The factors mediating fatal SARS-CoV-2 infections are poorly understood. This article shows that cigarette smoke causes a dose-dependent upregulation of Angiotensin Converting Enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, researchers demonstrates that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression.

In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, researchers demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, this work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive-feedback loops that increase ACE2 levels and facilitate viral dissemination.

Learning points:
-- Lung ACE2 levels do not vary by age or sex, but smokers exhibit upregulated ACE2.
-- ACE2 is expressed in several lung cell types, including the secretory lineage.
-- Chronic smoking triggers the expansion of ACE2+ secretory cells.
-- ACE2 is also upregulated by viral infections and interferon exposure.

Source: https://www.sciencedirect.com/science/article/pii/S1534580720304019
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