RT Journal Article
SR Electronic
T1 Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19
JF Science Immunology
JO Sci. Immunol.
FD American Association for the Advancement of Science
SP eabd1554
DO 10.1126/sciimmunol.abd1554
VO 5
IS 49
A1 Lee, Jeong Seok
A1 Park, Seongwan
A1 Jeong, Hye Won
A1 Ahn, Jin Young
A1 Choi, Seong Jin
A1 Lee, Hoyoung
A1 Choi, Baekgyu
A1 Nam, Su Kyung
A1 Sa, Moa
A1 Kwon, Ji-Soo
A1 Jeong, Su Jin
A1 Lee, Heung Kyu
A1 Park, Sung Ho
A1 Park, Su-Hyung
A1 Choi, Jun Yong
A1 Kim, Sung-Han
A1 Jung, Inkyung
A1 Shin, Eui-Cheol
YR 2020
UL http://immunology.sciencemag.org/content/5/49/eabd1554.abstract
AB By carrying out single-cell RNA sequencing analyses on immune cells in the blood, Lee et al. have compared immune responses in patients with mild and severe COVID-19 with immune responses in severe cases of influenza. They report TNF/IL-1β–driven inflammation as defining characteristics of COVID-19 that was relatively weak in the response to influenza. By further comparing the transcriptomes of mild and severe cases of COVID-19, they found type I interferons to be key drivers of inflammation in severe COVID-19. By profiling the immune responses to SARS-CoV-2 and flu in parallel, Lee et al. have shed new light on the similarities and differences between the immune responses to these two distinct respiratory viruses.Although most severe acute respiratory syndrome coronavirus 2 (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 sequencing 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 hyperinflammatory signatures across all types of cells among PBMCs, particularly up-regulation of the tumor necrosis factor/interleukin-1β (TNF/IL-1β)–driven inflammatory response as compared with severe influenza. In classical monocytes from patients with severe COVID-19, type I interferon (IFN) response coexisted with the TNF/IL-1β–driven inflammation, and this was not seen in patients with milder COVID-19. We documented type I IFN–driven inflammatory features in patients with severe influenza as well. On the basis of this, we propose that the type I IFN response plays a pivotal role in exacerbating inflammation in severe COVID-19.