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HGNC Genes

SARS-CoV-2 proteins

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    AXL HGNC Promotes SARS-CoV-2 Infection MESHD of Pulmonary and Bronchial Epithelial Cells

    Authors: Shuai Wang; Zongyang Qiu; Yingnan Hou; Xiya Deng; Tingting Zheng; Renhong Yan; Peihan Wu; Shaofang Xie; Qiang Zhou; Jing Huang; Xu Li

    doi:10.21203/rs.3.rs-35387/v1 Date: 2020-06-14 Source: ResearchSquare

    The current coronavirus disease 2019 MESHD ( COVID-19 MESHD) pandemic presents a global public health challenge. The viral pathogen responsible, Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), binds to a host receptor ACE2 HGNC through its spike ( S) glycoprotein PROTEIN, which mediates membrane fusion and virus entry. Although the role of ACE2 HGNC as a receptor for SARS-CoV-2 is clear, studies have shown that ACE2 HGNC expression across different human tissues is extremely low, especially in pulmonary and bronchial cells. Thus, other host receptors and/or co-receptors that promote the entry of SARS-CoV-2 into cells of the respiratory system might exist. In this study, we have identified tyrosine-protein kinase receptor UFO ( AXL HGNC), specifically interacts with SARS-CoV-2 S on the host cell membrane. When overexpressed in cells that do not highly express either AXL HGNC or ACE2 HGNC, AXL HGNC promotes virus entry as efficiently as ACE2 HGNC. Strikingly, deleting AXL HGNC, but not ACE2 HGNC, significantly reduces infection of pulmonary cells by the SARS-CoV-2 virus pseudotype. Soluble human recombinant AXL HGNC, but not ACE2 HGNC, blocks SARS-CoV-2 virus pseudotype infection in pulmonary cells. Taken together, our findings suggest AXL HGNC may play an important role in promoting SARS-CoV-2 infection MESHD of the human respiratory system and is a potential target in future clinical intervention strategies.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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