title: High susceptibility of human dendritic cells to avian influenza H5N1 virus infection and protection by IFN-alpha and TLR ligands.
abstract: There is worldwide concern that the avian influenza H5N1 virus, with a mortality rate of >50%, might cause the next influenza pandemic. Unlike most other influenza infections, H5N1 infection causes a systemic disease. The underlying mechanisms for this effect are still unclear. In this study, we investigate the interplay between avian influenza H5N1 and human dendritic cells (DC). We showed that H5N1 virus can infect and replicate in monocyte-derived and blood myeloid DC, leading to cell death. These results suggest that H5N1 escapes viral-specific immunity, and could disseminate via DC. In contrast, blood pDC were resistant to infection and produced high amounts of IFN-alpha. Addition of this cytokine to monocyte-derived DC or pretreatment with TLR ligands protected against infection and the cytopathic effects of H5N1 virus.
authors.affiliation: Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, Thailand.
authors.forename: Arunee
authors.initials: A
authors.lastname: Thitithanyanont
authors.forename: Anneke
authors.initials: A
authors.lastname: Engering
authors.forename: Peeraya
authors.initials: P
authors.lastname: Ekchariyawat
authors.forename: Suwimon
authors.initials: S
authors.lastname: Wiboon-ut
authors.forename: Amporn
authors.initials: A
authors.lastname: Limsalakpetch
authors.forename: Kosol
authors.initials: K
authors.lastname: Yongvanitchit
authors.forename: Utaiwan
authors.initials: U
authors.lastname: Kum-Arb
authors.forename: Watcharoot
authors.initials: W
authors.lastname: Kanchongkittiphon
authors.forename: Pongsak
authors.initials: P
authors.lastname: Utaisincharoen
authors.forename: Stitaya
authors.initials: S
authors.lastname: Sirisinha
authors.forename: Pilaipan
authors.initials: P
authors.lastname: Puthavathana
authors.forename: Mark M
authors.initials: MM
authors.lastname: Fukuda
authors.forename: Sathit
authors.initials: S
authors.lastname: Pichyangkul
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000378:metabolism; D001717:Birds; D019070:Cell Lineage / Q000276:immunology; D002478:Cells, Cultured; D018920:Coculture Techniques; D003588:Cytopathogenic Effect, Viral / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D004198:Disease Susceptibility / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D053124:Influenza A Virus, H5N1 Subtype / Q000276:immunology* / Q000472:pathogenicity; D005585:Influenza in Birds / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control; D016898:Interferon-alpha / Q000378:metabolism* / Q000502:physiology; D008024:Ligands; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology; D008969:Molecular Sequence Data; D009000:Monocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D051196:Toll-Like Receptor 3 / Q000378:metabolism / Q000502:physiology; D051197:Toll-Like Receptor 4 / Q000378:metabolism / Q000502:physiology; D051193:Toll-Like Receptors / Q000378:metabolism* / Q000502:physiology; D014779:Virus Replication / Q000276:immunology
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D008024:Ligands; D008070:Lipopolysaccharides; D051196:Toll-Like Receptor 3; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors