Osteopontin Impacts West Nile virus Pathogenesis and Resistance by Regulating Inflammasome Components and Cell Death in the Central Nervous System at Early Time Points

Figure 9

Schematic model for the role of OPN in WNV infection of the CNS. By delaying the induction of proinflammatory cytokines in vivo, OPN may act as a negative regulator of caspase 1-mediated apoptosis and IL1b, while promoting the induction of an alternative caspase 8 pathway. Conversely, in the absence of OPN, inflammatory cytokines are triggered soon after infection, activating caspase 1-mediated inflammasome components and ultimately resulting in an enrichment of caspase 3. As a result, cell death of infected cells may favor virus spread and further induction of secondary factors that aggravate the inflammatory pathogenesis in viral infections of the CNS, such as WNV.