Author: Kang, Chang Kyung; Choi, Baekgyu; Kim, Sugyeong; Park, Seongwan; Yoon, Soon Ho; Lee, Dohoon; Lee, Andrew J.; Ko, Yuji; Chang, Euijin; Jung, Jongtak; Choe, Pyoeng Gyun; Park, Wan Beom; Kim, Eu Suk; Kim, Hong Bin; Kim, Nam Joong; Oh, Myoung-don; Kang, Suk-jo; Kang, Kyuho; Kim, Sun; Im, Hogune; Kim, Joohae; Lee, Yong Hoon; Lee, Jaehee; Lee, Ji Yeon; Moon, Joon Ho; Song, Kyoung-Ho; Koh, Youngil; Jung, Inkyung
Title: Clinical and immunological signatures of severe COVID-19 in previously healthy patients with clonal hematopoiesis Cord-id: 8gy35crg Document date: 2021_10_9
ID: 8gy35crg
Snippet: Identifying additional risk factors for COVID-19 severity in numerous previously healthy patients without canonical clinical risk factors remains challenging. In this study, we investigate whether clonal hematopoiesis of indeterminate potential (CHIP), a common aging-related process that predisposes various inflammatory responses, may exert COVID-19 severity. We examine the clinical impact of CHIP in 143 laboratory-confirmed COVID-19 patients. Both stratified analyses and logistic regression inc
Document: Identifying additional risk factors for COVID-19 severity in numerous previously healthy patients without canonical clinical risk factors remains challenging. In this study, we investigate whether clonal hematopoiesis of indeterminate potential (CHIP), a common aging-related process that predisposes various inflammatory responses, may exert COVID-19 severity. We examine the clinical impact of CHIP in 143 laboratory-confirmed COVID-19 patients. Both stratified analyses and logistic regression including the interaction between canonical risk factors and CHIP show that CHIP is an independent risk factor for severe COVID-19, especially in previously healthy patients. Analyses of 60,310 single-cell immune transcriptome profiles identify distinct immunological signatures for CHIP (+) severe COVID-19 patients, particularly in classical monocytes, with a marked increase in pro-inflammatory cytokine responses and potent IFN-γ mediated hyperinflammation signature. We further demonstrate that the enhanced expression of CHIP (+) specific IFN-γ response genes is attributed to the CHIP mutation-dependent epigenetic reprogramming of poised or bivalent cis-regulatory elements. Our results highlight a unique immunopathogenic mechanism of CHIP in the progression of severe COVID-19, which could be extended to elucidate how CHIP contributes to a variety of human infectious diseases.
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