Abstract
Avian influenza A (H7N9) virus infections frequently lead to acute respiratory distress syndrome and death in humans. The emergence of H7N9 virus infections is a serious public health threat. To identify virus–host interaction differences between the highly virulent H7N9 and pandemic influenza H1N1 (pdmH1N1), RNA sequencing was performed of normal human bronchial epithelial (NHBE) cells infected with either virus. The transcriptomic analysis of host cellular responses to viral infection enables the identification of potential cellular factors related to infection. Significantly different gene expression patterns were found between pdmH1N1- and H7N9-infected NHBE cells. In addition, the H7N9 virus infection induced strong immune responses, while cellular repair mechanisms were inhibited. The differential expression of specific factors observed between avian H7N9 and pdmH1N1 influenza virus strains can account for variations in disease pathogenicity. These findings provide a framework for future studies examining the molecular mechanisms underlying the pathogenicity of avian H7N9 virus.
Highlights
The influenza A virus is a negative-sense, single-stranded, and enveloped RNA virus that belongs to the Orthomyxoviridae family
These findings provide a framework for future studies examining the molecular mechanisms underlying the pathogenicity of avian H7N9 virus
We found that H7N9 infection induced the expression of chemokines IL-8, IP-10, and RANTES in normal human bronchial epithelial (NHBE) cells and reduced the expression of MIP-1β, eotaxin, monocyte chemotactic protein 1 (MCP-1), and macrophage inflammatory protein 1α (MIP-1α)
Summary
The influenza A virus is a negative-sense, single-stranded, and enveloped RNA virus that belongs to the Orthomyxoviridae family. Avian-origin influenza A H7N9 infection in humans was initially reported in China in March 2013 [4,5,6]. The ability of the avian influenza virus to break the species barrier and infect humans is determined by HA and PB2. Avian influenza A H7N9 virus infections frequently lead to acute respiratory distress syndrome, multiorgan disfunction, shock, and death in humans; there were 133 laboratory-confirmed H7N9 virus cases in March to July 2013, with 43 deaths reported, giving a case fatality of 32%. We determined that H7N9 virus infection induced a strong immune response, while inhibiting cellular repair mechanisms. These findings provide a framework for future studies examining the molecular mechanisms underlying the pathogenicity of avian H7N9 virus
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