PropertyValue
?:abstract
  • Studies of SARS-CoV-2-infected patients and experimentally infected animals indicate a critical role for augmented expression of pro-inflammatory chemokines and cytokines in severe disease. Here, we demonstrate that SARS-CoV-2 infection of human monocyte-derived macrophages (MDMs) and dendritic cells (MDDCs) was abortive, but induced the production of multiple antiviral and pro-inflammatory cytokines (IFN-α, IFN-β, TNF, IL-1β, IL-6 and IL-10) and a chemokine (CXCL10). Despite the lack of efficient replication in MDMs, SARS-CoV-2 induced profound IFN-mediated cell death of host cells. Macrophage activation and death was not enhanced by exposure to low levels of convalescent plasma, suggesting that antibody-dependent enhancement of infection does not contribute to cell death. Together, these results indicate that infection of macrophages and dendritic cells potentially plays a major role in COVID-19 pathogenesis, even in the absence of productive infection.
is ?:annotates of
?:creator
?:doi
  • 10.1093/infdis/jiaa753
?:doi
?:journal
  • J_Infect_Dis
?:license
  • no-cc
?:pdf_json_files
  • document_parses/pdf_json/04dbf436933eb4de4c4d46c4c1f6b794d0fbafb7.json
?:pmcid
?:pmid
?:pmid
  • 33277988.0
?:publication_isRelatedTo_Disease
?:sha_id
?:source
  • Medline; PMC
?:title
  • SARS-CoV-2-induced immune activation and death of monocyte-derived human macrophages and dendritic cells
?:type
?:year
  • 2020-12-05

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