Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 222, Issue 5, Pages 734-745Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiaa356
Keywords
COVID-19; SARS-CoV-2; coronavirus; dendritic cells; macrophages; moDCs; MDMs
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Funding
- Shaw Foundation of Hong Kong
- Respiratory Viral Research Foundation Limited
- Hui Ming, Hui Hoy and Chow Sin Lan Charity Fund Limited
- Chan Yin Chuen Memorial Charitable Foundation
- Hong Kong Hainan Commercial Association South China Microbiology Research Fund
- Jessie and George Ho Charitable Foundation
- Perfect Shape Medical Limited
- Lo Ying Shek Chi Wai Foundation
- Kai Chong Tong
- Consultancy Service for Enhancing Laboratory Surveillance of Emerging Infectious Diseases and Research Capability on Antimicrobial Resistance, Department of Health, Hong Kong Special Administrative Region
- Research Grants Council, Hong Kong Special Administrative Region, Theme-Based Research Scheme [T11/707/15]
- Sanming Project of Medicine in Shenzhen, China [SZSM201911014]
- High Level-Hospital Program, Health Commission of Guangdong Province, China
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Clinical manifestations of coronavirus disease 2019 (COVID-19) vary from asymptomatic virus shedding, nonspecific pharyngitis, to pneumonia with silent hypoxia and respiratory failure. Dendritic cells and macrophages are sentinel cells for innate and adaptive immunity that affect the pathogenesis of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). The interplay between SARS-CoV-2 and these cell types remains unknown. We investigated infection and host responses of monocyte-derived dendritic cells (moDCs) and macrophages (MDMs) infected by SARS-CoV-2. MoDCs and MDMs were permissive to SARS-CoV-2 infection and protein expression but did not support productive virus replication. Importantly, SARS-CoV-2 launched an attenuated interferon response in both cell types and triggered significant proinflammatory cytokine/chemokine expression in MDMs but not moDCs. Investigations suggested that this attenuated immune response to SARS-CoV-2 in moDCs was associated with viral antagonism of STAT1 phosphorylation. These findings may explain the mild and insidious course of COVID-19 until late deterioration.
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