Bo Zhang

TL;DR: It is demonstrated that in response to WNV infection, neurons secrete theChemokine CXCL10, which recruits effector T cells via the chemokine receptor CXCR3, which leads to a decrease in CX CR3+ CD8+ T-cell trafficking, an increase in viral burden in the brain, and enhanced morbidity and mortality.

TL;DR: Results indicate that WNV differentially induces CXCL10 within neuronal populations and suggest a novel model for nonredundancy in chemokine-mediated inflammation among CNS compartments.

TL;DR: Antagonism of CXCR4 significantly improved survival from lethal infection through enhanced intraparenchymal migration of WNV-specific CD8+ T cells within the brain, leading to reduced viral loads and, surprisingly, decreased immunopathology at this site.

TL;DR: The authors' data are most consistent with a model in which interaction of TNF-α with T NF-R1 protects against WNV infection by regulating migration of protective inflammatory cells into the brain during acute infection.

TL;DR: Using a murine model of West Nile virus (WNV) encephalitis, it is determined that WNV-infected neurons express TNF-alpha, which down-regulates neuronal CXCR3 expression via signaling through TNFR1, which suggests that neuronal T NF-alpha expression during WNVEncephalitis may be an adaptive response to diminish CXCL10-induced death.