Distinct infection process of SARS‐CoV‐2 in human bronchial epithelial cells line

Liao, Yun; Li, Xueqi; Mou, Tangwei; Zhou, Xiaofang; Li, Dandan; Wang, Lichun; Zhang, Ying; dong, Xingqi; Zheng, Huiwen; Guo, Lei; Liang, Yan; Jiang, Guorun; Fan, Shengtao; Xu, Xingli; Xie, Zhongping; Chen, Hongbo; Liu, Longding; Li, Qihan

COVID‐19, caused by SARS‐CoV‐2, leads to a series of clinical symptoms of respiratory and pulmonary inflammatory reactions via unknown pathologic mechanisms related to the viral infection process in tracheal or bronchial epithelial cells. Investigation of this viral infection in the human bronchial epithelial cell line (16HBE) suggests that SARS‐CoV‐2 can enter these cells through interaction between its membrane‐localized S protein with the ACE2 molecule on the host cell membrane. Further observation indicates distinct viral replication with a dynamic and moderate increase, whereby viral replication does not lead to a specific cytopathic effect but maintains a continuous release of progeny virions from infected cells. Although mRNA expression of various innate immune signaling molecules is altered in the cells, transcription of IFNα, IFNβ and IFNγ is unchanged. Furthermore, expression of some interleukins related to inflammatory reactions, such as IL‐6, IL‐2 and IL‐8, is maintained at low levels, whereas that of interleukins involved in immune regulation is upregulated. Interestingly, IL‐22, an interleukin that functions mainly in tissue repair, shows very high expression. Collectively, these data suggest a distinct infection process for this virus in respiratory epithelial cells, which may be linked to its clinicopathological mechanism. This article is protected by copyright. All rights reserved.