Temporal omics analysis in Syrian hamsters unravel cellular effector responses to moderate COVID-19


  • G. Nouailles
  • E. Wyler
  • P. Pennitz
  • D. Postmus
  • D. Vladimirova
  • J. Kazmierski
  • F. Pott
  • K. Dietert
  • M. Muelleder
  • V. Farztdinov
  • B. Obermayer
  • S.M. Wienhold
  • S. Andreotti
  • T. Hoefler
  • B. Sawitzki
  • C. Drosten
  • L.E. Sander
  • N. Suttorp
  • M. Ralser
  • D. Beule
  • A.D. Gruber
  • C. Goffinet
  • M. Landthaler
  • J. Trimpert
  • M. Witzenrath


  • Nature Communications


  • Nat Commun 12 (1): 4869


  • In COVID-19, immune responses are key in determining disease severity. However, cellular mechanisms at the onset of inflammatory lung injury in SARS-CoV-2 infection, particularly involving endothelial cells, remain ill-defined. Using Syrian hamsters as a model for moderate COVID-19, we conduct a detailed longitudinal analysis of systemic and pulmonary cellular responses, and corroborate it with datasets from COVID-19 patients. Monocyte-derived macrophages in lungs exert the earliest and strongest transcriptional response to infection, including induction of pro-inflammatory genes, while epithelial cells show weak alterations. Without evidence for productive infection, endothelial cells react, depending on cell subtypes, by strong and early expression of anti-viral, pro-inflammatory, and T cell recruiting genes. Recruitment of cytotoxic T cells as well as emergence of IgM antibodies precede viral clearance at day 5 post infection. Investigating SARS-CoV-2 infected Syrian hamsters thus identifies cell type-specific effector functions, providing detailed insights into pathomechanisms of COVID-19 and informing therapeutic strategies.