Innate immune responses to influenza A H5N1: friend or foe?
Avian influenza A H5N1 remains unusual in its virulence for humans. Although infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia that leads to acute respiratory distress syndrome and death, but its pathogenesis remains an enigma. Comparison of the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and relevant primary human cell cultures is instructive. Although the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease.
Department of Microbiology, University Pathology Building, Queen Mary Hospital, Pokfulam, Hong Kong SAR. malik@hkucc.hku.hk
Joseph Sriyal Malik
JS
Peiris
Chung Yan
CY
Cheung
Connie Yin Hung
CY
Leung
John Malcolm
JM
Nicholls
D000818:Animals; D006801:Humans; D007113:Immunity, Innate; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology / Q000472:pathogenicity; D053122:Influenza A Virus, H3N2 Subtype / Q000276:immunology / Q000472:pathogenicity; D053124:Influenza A Virus, H5N1 Subtype / Q000276:immunology* / Q000472:pathogenicity; D007251:Influenza, Human / Q000453:epidemiology / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D007372:Interferons / Q000378:metabolism; D051379:Mice; D009976:Orthomyxoviridae Infections / Q000276:immunology / Q000503:physiopathology; D012128:Respiratory Distress Syndrome / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D014409:Tumor Necrosis Factor-alpha; D007372:Interferons