Research Press Release

SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes

Nature Medicine

April 24, 2020

Multi-tissue genetic analysis suggests SARS-CoV-2 may infect specific nose cells Genes associated with how the virus SARS-CoV-2 enters a host were found to be expressed in specific healthy human respiratory, corneal and intestinal epithelial cells, according to a paper published this week in Nature Medicine. Expression of these genes was observed in nasal cells alongside that of genes involved in the innate immune system, which suggests a potential role for nasal tissue in initial viral infection, transmission and clearance.

Previous research had shown that nasal swabs from patients with symptomatic or asymptomatic COVID-19 respiratory disease (the disease caused by SARS-CoV-2) exhibit higher viral concentrations than those in throat swabs. This has implicated the nasal passage as a potential gateway for initial infection and transmission.

ACE2 and TMPRSS2 are two molecules involved in SARS-CoV-2 viral entry. To clarify the expression patterns of the genes encoding ACE2 and TMPRSS2, Waradon Sungnak and colleagues from the Lung Biological Network examined various human tissue samples obtained from healthy donors. The authors analysed data for tissues from various parts of the respiratory system, the retina, skeletal muscle, prostate, brain and skin, among other locations. They confirmed the expression of ACE2 in multiple tissues implicated in prior research. They also detected ACE2 expression in tissues not previously analysed, along with its co-expression with TMPRSS2.

The authors found high expression of ACE2 and TMPRSS2 in nasal goblet and ciliated cells, which produce mucus. This suggests that these cells are the location of original viral infection and are possibly the source of dissemination within and between people.

The authors conclude that their results could potentially have implications for future treatment and prevention of COVID-19.

doi:10.1038/s41591-020-0868-6

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