A human coronavirus responsible for the common cold massively kills dendritic cells but not monocytes

J Virol. 2012 Jul;86(14):7577-87. doi: 10.1128/JVI.00269-12. Epub 2012 May 2.


Human coronaviruses are associated with upper respiratory tract infections that occasionally spread to the lungs and other organs. Although airway epithelial cells represent an important target for infection, the respiratory epithelium is also composed of an elaborate network of dendritic cells (DCs) that are essential sentinels of the immune system, sensing pathogens and presenting foreign antigens to T lymphocytes. In this report, we show that in vitro infection by human coronavirus 229E (HCoV-229E) induces massive cytopathic effects in DCs, including the formation of large syncytia and cell death within only few hours. In contrast, monocytes are much more resistant to infection and cytopathic effects despite similar expression levels of CD13, the membrane receptor for HCoV-229E. While the differentiation of monocytes into DCs in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4 requires 5 days, only 24 h are sufficient for these cytokines to sensitize monocytes to cell death and cytopathic effects when infected by HCoV-229E. Cell death induced by HCoV-229E is independent of TRAIL, FasL, tumor necrosis factor alpha, and caspase activity, indicating that viral replication is directly responsible for the observed cytopathic effects. The consequence of DC death at the early stage of HCoV-229E infection may have an impact on the early control of viral dissemination and on the establishment of long-lasting immune memory, since people can be reinfected multiple times by HCoV-229E.

MeSH terms

  • Antigens, CD34 / analysis
  • CD13 Antigens / analysis
  • Caspases / metabolism
  • Cell Death
  • Common Cold / virology*
  • Coronavirus 229E, Human / pathogenicity*
  • Coronavirus 229E, Human / physiology
  • Cytopathogenic Effect, Viral*
  • Dendritic Cells / pathology
  • Dendritic Cells / virology*
  • Fas Ligand Protein / metabolism
  • Giant Cells / pathology
  • Giant Cells / virology
  • Humans
  • Monocytes / immunology
  • Monocytes / pathology
  • Monocytes / virology*
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / virology*
  • TNF-Related Apoptosis-Inducing Ligand / metabolism
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / metabolism
  • Virus Replication


  • Antigens, CD34
  • FASLG protein, human
  • Fas Ligand Protein
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human
  • Tumor Necrosis Factor-alpha
  • CD13 Antigens
  • Caspases