Even though infection by both mutated and wild-type viruses led to neuroinflammation, the modified neuropathogenesis induced by the mutated virus was associated with increased viral spread and significantly more CD4+ and CD8+ T-lymphocyte infiltration into the central nervous system, as well as significantly increased levels of the pro-inflammatory cytokine IL 6 and the chemokine CCL2 (MCP-1), and a trend towards increases in cytokines TNF-alpha, and IFN-gamma and chemokines CCL5 (RANTES) and CXCL10 (IP-10).