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

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  • Cell Host Microbe. Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients


    Cell Host Microbe. 2020 May 4. pii: S1931-3128(20)30244-4. doi: 10.1016/j.chom.2020.04.017. [Epub ahead of print]
    Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients.


    Zhou Z1, Ren L2, Zhang L3, Zhong J4, Xiao Y5, Jia Z6, Guo L5, Yang J4, Wang C4, Jiang S3, Yang D7, Zhang G8, Li H9, Chen F10, Xu Y7, Chen M11, Gao Z7, Yang J5, Dong J5, Liu B5, Zhang X12, Wang W6, He K6, Jin Q5, Li M13, Wang J14.

    Author information




    Abstract

    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.
    Copyright ? 2020 Elsevier Inc. All rights reserved.



    KEYWORDS:

    Bronchoalveolar lavage fluid; COVID-19; Chemokines; Coronavirus; Hypercytokinemia; Innate immune response; Interferon response; Interferon-stimulated genes; Metatranscriptomic sequencing; SARS-CoV-2


    PMID:32407669DOI:10.1016/j.chom.2020.04.017

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