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Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients.

Authors: Zhou, Zhuo  Ren, Lili  Zhang, Li  Zhong, Jiaxin  Xiao, Yan  Jia, Zhilong  Guo, Li  Yang, Jing  Wang, Chun  Jiang, Shuai  Yang, Donghong  Zhang, Guoliang  Li, Hongru  Chen, Fuhui  Xu, Yu  Chen, Mingwei  Gao, Zhancheng  Yang, Jian  Dong, Jie  Liu, Bo  Zhang, Xiannian  Wang, Weidong  He, Kunlun  Jin, Qi  Li, Mingkun  Wang, Jianwei 
Citation: Zhou Z, etal., Cell Host Microbe. 2020 Jun 10;27(6):883-890.e2. doi: 10.1016/j.chom.2020.04.017. Epub 2020 May 4.
Pubmed: (View Article at PubMed) PMID:32407669
DOI: Full-text: DOI:10.1016/j.chom.2020.04.017

The outbreaks of 2019 novel coronavirus disease (COVID-19) caused by SARS-CoV-2 infection have posed a severe threat to global public health. It is unclear how the human immune system responds to this infection. Here, we used metatranscriptomic sequencing to profile immune signatures in the bronchoalveolar lavage fluid of eight COVID-19 cases. The expression of proinflammatory genes, especially chemokines, was markedly elevated in COVID-19 cases compared to community-acquired pneumonia patients and healthy controls, suggesting that SARS-CoV-2 infection causes hypercytokinemia. Compared to SARS-CoV, which is thought to induce inadequate interferon (IFN) responses, SARS-CoV-2 robustly triggered expression of numerous IFN-stimulated genes (ISGs). These ISGs exhibit immunopathogenic potential, with overrepresentation of genes involved in inflammation. The transcriptome data was also used to estimate immune cell populations, revealing increases in activated dendritic cells and neutrophils. Collectively, these host responses to SARS-CoV-2 infection could further our understanding of disease pathogenesis and point toward antiviral strategies.

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CRRD Object Information
CRRD ID: 30296672
Created: 2020-06-16
Species: All species
Last Modified: 2020-06-16
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.