Abstract
In March 2013 a new avian influenza A(H7N9) virus emerged in China and infected humans with a case fatality rate of over 30%. Like the highly pathogenic H5N1 virus, H7N9 virus is causing severe respiratory distress syndrome in most patients. Based on genetic analysis this avian influenza A virus shows to some extent adaptation to mammalian host. In the present study, we analyzed the activation of innate immune responses by this novel H7N9 influenza A virus and compared these responses to those induced by the avian H5N1 and seasonal H3N2 viruses in human monocyte-derived dendritic cells (moDCs). We observed that in H7N9 virus-infected cells, interferon (IFN) responses were weak although the virus replicated as well as the H5N1 and H3N2 viruses in moDCs. H7N9 virus-induced expression of pro-inflammatory cytokines remained at a significantly lower level as compared to H5N1 virus-induced “cytokine storm” seen in human moDCs. However, the H7N9 virus was extremely sensitive to the antiviral effects of IFN-α and IFN-β in pretreated cells. Our data indicates that different highly pathogenic avian viruses may show considerable differences in their ability to induce host antiviral responses in human primary cell models such as moDCs. The unexpected appearance of the novel H7N9 virus clearly emphasizes the importance of the global influenza surveillance system. It is, however, equally important to systematically characterize in normal human cells the replication capacity of the new viruses and their ability to induce and respond to natural antiviral substances such as IFNs.
Highlights
In spring 2013 a novel avian influenza A (H7N9) virus emerged in eastern China and by March 2014 has caused two epidemic cluster with nearly 400 reported infections with a mortality of more that 30% [1]
We analyzed the ability of the novel avian-origin H7N9 virus strain A/Anhui/1/13, highly pathogenic avian influenza (HPAI) A/Vietnam/1194/04 (H5N1) virus and the seasonal A/Beijing/353/89 (H3N2) virus to replicate and induce immune responses in human primary monocyte-derived dendritic cells (moDCs)
Equivalent amounts of infective viruses were used to infect human moDCs. This amount represented a multiplicity of infection (MOI) of 1 for H3N2 virus strain in moDCs that was determined previously [19]
Summary
In spring 2013 a novel avian influenza A (H7N9) virus emerged in eastern China and by March 2014 has caused two epidemic cluster with nearly 400 reported infections with a mortality of more that 30% [1]. Many avian influenza viruses circulate endemically in poultry and occasionally cause sporadic infections in humans that are in close contact with live birds at markets or farms, H7N9 virus strain has never before found in humans. The novel H7N9 virus appears to be an exception, since it appears to be low pathogenic in birds but highly pathogenic in humans. Most H7N9 virus-infected patients developed severe pneumonia and acute respiratory distress syndrome (ARDS) [2,3]. It is of great concern if the virus would acquire the ability for sustained human-to-human transmission. Further characterization of the specific properties of this novel virus such as the molecular determinants of pathogenesis, factors contributing to the ability to replicate in mammalian host, virus – host cell interactions and sensitivity to antiviral substances are of great importance
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