interleukin-8 and West-Nile-Fever

West Nile virus (WNV) circulates across Australia and was referred to historically as Kunjin virus (WNV. To better understand the emergence of this virulent phenotype and the mechanism by which pathogenicity is manifested in its host, cells were infected with either the virulent strain (NSW2012), or less pathogenic historical isolates, and their innate immune responses compared by digital immune gene expression profiling. Two different cell systems were used: a neuroblastoma cell line (SK-N-SH cells) and neuronal cells derived from induced pluripotent stem cells (iPSCs).. Significant innate immune gene induction was observed in both systems. The NSW2012 isolate induced higher gene expression of two genes (IL-8 and CCL2) when compared with cells infected with less pathogenic isolates. Pathway analysis of induced inflammation-associated genes also indicated generally higher activation in infected NSW2012 cells. However, this differential response was not paralleled in the neuronal cultures.. NSW2012 may have unique genetic characteristics which contributed to the outbreak. The data herein is consistent with the possibility that the virulence of NSW2012 is underpinned by increased induction of inflammatory genes.

Topics: Australia; Cell Line, Tumor; Chemokine CCL2; Disease Outbreaks; Gene Expression; Gene Expression Profiling; Humans; Immunity, Innate; Induced Pluripotent Stem Cells; Inflammation; Interleukin-8; Neurons; Phenotype; Virulence; West Nile Fever; West Nile virus