한빛사 논문
Jeong Seok Lee1*, Seongwan Park2*, Hye Won Jeong3*, Jin Young Ahn4*, Seong Jin Choi1, Hoyoung Lee1, Baekgyu Choi2, Su Kyung Nam2, Moa Sa1,5, Ji-Soo Kwon1,6, Su Jin Jeong4, Heung Kyu Lee1,5, Sung Ho Park7, Su-Hyung Park1,5, Jun Yong Choi4†, Sung-Han Kim6†, Inkyung Jung2†, Eui-Cheol Shin1,5†
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
2Department of Biological Sciences, KAIST, Daejeon 34141, Republic of Korea. 3Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju 28644, Republic of Korea.
4Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
5The Center for Epidemic Preparedness, KAIST Institute, Daejeon 34141, Republic of Korea.
6Department of Infectious Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Republic of Korea.
7School of Life Sciences, Ulsan National Institute of Science & Technology (UNIST), Ulsan 44919, Republic of Korea.
*Theses authors contributed equally to this work.
†Corresponding author
Abstract
Although most SARS-CoV-2-infected individuals experience mild coronavirus disease 2019 (COVID-19), some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly up-regulation of the TNF/IL-1β-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1β-driven inflammation, and this was not seen in patients with milder COVID-19. Interestingly, we documented type I IFN-driven inflammatory features in patients with severe influenza as well. Based on this, we propose that the type I IFN response plays a pivotal role in exacerbating inflammation in severe COVID-19.
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