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MeSH Disease

Human Phenotype

Transmission

Seroprevalence

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    A Hint on the COVID-19 Risk: Population Disparities in Gene Expression of Three Receptors of SARS-CoV MESHD

    Authors: Guoshuai Cai; Xiang Cui; Xia Zhu; Jun Zhou

    id:10.20944/preprints202002.0408.v1 Date: 2020-02-27 Source: Preprints.org

    The current spreading novel coronavirus SARS-CoV-2 is highly infectious and pathogenic and has attracted global attention. Recent studies have found that SARS-CoV-2 and SARS-CoV share around 80% of homology and use the same cell entry receptor, ACE2. These inspired us to study other receptors of SARS-CoV MESHD, which may be used for SARS-CoV-2 binding as well. In this study, we screened the gene expression of three receptors (ACE2, DC-SIGN and L-SIGN) in four datasets of normal lung tissue from lung adenocarcinoma HP patients and two single-cell RNA sequencing datasets from normal lung and bronchial epithelial cells separately. No significant difference in gene expression of these three receptors were found between gender TRANS groups ( male TRANS vs female TRANS). We found higher gene expression of DC-SIGN in elder with age TRANS>60 and higher gene expression of L-SIGN in Caucasian than Asian. Similar to ACE2, we observed significantly higher DC-SIGN gene expression in the lungs of smokers, especially former smokers. However, smokers upregulate ACE2 and DC-SIGN gene expression in different cell types. In the whole lung, ACE2 is actively expressed in remodeled Alveolar Type II MESHD cells of former smokers, while DC-SIGN is largely expressed in monocytes of former smokers and dendritic cells of current smokers. In bronchial epithelium, no obvious gene expression of DC-SIGN and L-SIGN was observed while ACE2 was found to be actively expressed in goblet cells of current smokers and club HP cells of non-smokers. In conclusion, our findings may indicate that smokers, especially former smokers, and people over 60 have higher risk and are more susceptible to SARS-CoV-2 infection MESHD. Also, this study provides hints on possible SARS-CoV-2 pathogenicity mechanisms in lung infection MESHD.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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