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SARS-CoV-2 Infection of Airway Epithelial CellsSARS-CoV-2 Infection of Airway Epithelial Cells

Other Titles
SARS-CoV-2 Infection of Airway Epithelial Cells
Authors
Ryu, GwanghuiShin, Hyun-Woo
Issue Date
Feb-2021
Publisher
대한면역학회
Keywords
COVID-19; Coronavirus; SARS-CoV-2; Respiratory system; Epithelial cells
Citation
Immune Network, v.21, no.1, pp 1 - 16
Pages
16
Journal Title
Immune Network
Volume
21
Number
1
Start Page
1
End Page
16
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/2048
DOI
10.4110/in.2021.21.e3
ISSN
1598-2629
2092-6685
Abstract
Coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been spreading worldwide since its outbreak in December 2019, and World Health Organization declared it as a pandemic on March 11, 2020. SARS-CoV-2 is highly contagious and is transmitted through airway epithelial cells as the first gateway. SARS-CoV-2 is detected by nasopharyngeal or oropharyngeal swab samples, and the viral load is significantly high in the upper respiratory tract. The host cellular receptors in airway epithelial cells, including angiotensin-converting enzyme 2 and transmembrane serine protease 2, have been identified by single-cell RNA sequencing or immunostaining. The expression levels of these molecules vary by type, function, and location ofairway epithelial cells, such as ciliated cells, secretory cells, olfactory epithelial cells, and alveolar epithelial cells, as well as differ from host to host depending on age, sex, or comorbid diseases. Infected airway epithelial cells by SARS-CoV-2 in ex vivo experiments produce chemokines and cytokines to recruit inflammatory cells to target organs. Same as other viral infections, IFN signaling is a critical pathway for host defense. Various studies are underway to confirm the pathophysiological mechanisms of SARS-CoV-2 infection. Herein, we review cellular entry, host-viral interactions, immune responses to SARS-CoV-2 in airway epithelial cells. We also discuss therapeutic options related to epithelial immune reactions to SARS-CoV-2.
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