Abstract
Infection of chickens with low pathogenicity avian influenza (LPAI) virus results in mild clinical signs while infection with highly pathogenic avian influenza (HPAI) viruses causes death of the birds within 36–48 hours. Since natural killer (NK) cells have been shown to play an important role in influenza-specific immunity, we hypothesise that NK cells are involved in this difference in pathogenicity. To investigate this, the role of chicken NK-cells in LPAI virus infection was studied. Next activation of lung NK cells upon HPAI virus infection was analysed. Infection with a H9N2 LPAI virus resulted in the presence of viral RNA in the lungs which coincided with enhanced activation of lung NK cells. The presence of H5N1 viruses, measured by detection of viral RNA, did not induce activation of lung NK cells. This suggests that decreased NK-cell activation may be one of the mechanisms associated with the enhanced pathogenicity of H5N1 viruses.
Highlights
Infection of chickens with low pathogenicity avian influenza (LPAI) virus results in mild clinical signs while infection with highly pathogenic avian influenza (HPAI) viruses causes death of the birds within 36–48 hours
In the present study we hypothesise that the lack of natural killer (NK)-cell activation induced by H5N1 viruses is a property of these viruses, and that the diminished NK-cell activation upon infection with highly pathogenic avian influenza virus is associated with enhanced pathogenicity
Since avian influenza viruses use a distinct binding site on NKp46 compared to the human and swine influenza viruses and binding is dependent on a2,3-SA rather than a2,6-SA residues on the receptor[34], the lack of NK-cell cytotoxicity upon binding of avian H5N1 virus to human NKp46 itself in the absence of NKG2D crosslinking may be due to differences in receptor specificity
Summary
Infection of chickens with low pathogenicity avian influenza (LPAI) virus results in mild clinical signs while infection with highly pathogenic avian influenza (HPAI) viruses causes death of the birds within 36–48 hours. Killing of H5N1 infected targets is only observed when both NKp46 and NKG2D are activated[34] This lack of NK-cell activation upon the interaction between H5N1 avian influenza viruses and NKp46 itself may be a property of these viruses which contributes to www.nature.com/scientificreports their highly pathogenic nature. It may be caused by the fact that the interactions between avian H5N1 virus and the human NKp46 through its a2,3-SA are insufficient to induce killing by NK cells. In the present study we hypothesise that the lack of NK-cell activation induced by H5N1 viruses is a property of these viruses, and that the diminished NK-cell activation upon infection with highly pathogenic avian influenza virus is associated with enhanced pathogenicity
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