Insights into the increasing virulence of the swine-origin pandemic H1N1/2009 influenza virus.
Sci Rep, 2013;3:1601.
Zou W[1], Chen D, Xiong M, Zhu J, Lin X, Wang L, Zhang J, Chen L, Zhang H, Chen H, Chen M, Jin M
Affiliations
PMID: 23549303DOI: 10.1038/srep01601
Impact factor: 4.996
Abstract
Pandemic H1N1/2009 viruses have been stabilized in swine herds, and some strains display higher pathogenicity than the human-origin isolates. In this study, high-throughput RNA sequencing (RNA-seq) is applied to explore the systemic transcriptome responses of the mouse lungs infected by swine (Jia6/10) and human (LN/09) H1N1/2009 viruses. The transcriptome data show that Jia6/10 activates stronger virus-sensing signals, such as the toll-like receptor, RIG-I like receptor and NOD-like receptor signalings, as well as a stronger NF-κB and JAK-STAT signals, which play significant roles in inducing innate immunity. Most cytokines and interferon-stimulated genes show higher expression lever in Jia/06 infected groups. Meanwhile, virus Jia6/10 activates stronger production of reactive oxygen species, which might further promote higher mutation rate of the virus genome. Collectively, our data reveal that the swine-origin pandemic H1N1/2009 virus elicits a stronger innate immune reaction and pro-oxidation stimulation, which might relate closely to the increasing pathogenicity.
MeSH terms
Animals; Humans; Influenza A Virus, H1N1 Subtype; Influenza, Human; Lung; Mice; Molecular Sequence Data; Pandemics; Swine; Transcriptome; Virulence; Virulence Factors
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