Distinct infection process of SARS-CoV-2 in human bronchial epithelial cells line
Distinct infection process of SARS-CoV-2 in human bronchial epithelial cells line
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DOI：
10.1002/jmv.26200
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发表时间：
2020-07-14
影响因子：
12.7
通讯作者：
Li, Qihan
中科院分区：
文献类型：
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作者：
Liao, Yun;Li, Xueqi;Li, Qihan
由严重急性呼吸综合征冠状病毒-2（SARS-CoV-2）引起的2019冠状病毒病通过与气管或支气管上皮细胞中病毒感染过程相关的未知病理机制导致一系列呼吸道和肺部炎症反应的临床症状。对这种病毒感染人支气管上皮细胞系（16 HBE）的研究表明，SARS-CoV-2可以通过其膜定位的S蛋白与宿主细胞膜上的血管紧张素转换酶2分子之间的相互作用进入这些细胞。进一步的观察表明，不同的病毒复制具有动态和适度的增加，由此病毒复制不会导致特定的细胞病变效应，而是保持子代病毒体从感染细胞中的连续释放。尽管细胞中各种先天免疫信号分子的信使RNA表达发生改变，但干扰素-α（IFN-α）、IFN-β和IFN-γ的转录没有改变。此外，一些与炎症反应相关的白细胞介素（IL），如IL-6，IL-2和IL-8的表达维持在低水平，而参与免疫调节的IL的表达上调。有趣的是，IL-22，一种主要在组织修复中起作用的IL，显示出非常高的表达。总的来说，这些数据表明这种病毒在呼吸道上皮细胞中的独特感染过程，这可能与其临床病理机制有关。
Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus-2 (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 angiotensin-converting enzyme 2 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 messenger RNA expression of various innate immune signaling molecules is altered in the cells, transcription of interferons-alpha (IFN-alpha), IFN-beta, and IFN-gamma is unchanged. Furthermore, expression of some interleukins (IL) related to inflammatory reactions, such as IL-6, IL-2, and IL-8, is maintained at low levels, whereas that of ILs involved in immune regulation is upregulated. Interestingly, IL-22, an IL 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.