Infection of CNS tissue with WNV in vivo [21,58] and in ex vivo [41] and in vitro [23] models of WNV pathogenesis results in increased expression of proinflammatory cytokines and chemokines associated with microglial activation including C-X-C motif chemokine 10 (CXCL10), CXCL1, CCL5, CCL3, CCL2, tumor necrosis factor alpha (TNF-α), TNF-related apoptosis-inducing ligand (TRAIL), and interleukin-6 (IL-6) [40]. The gene discussed is CCL2; the disease is infection.