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More than 50% of West Nile virus (WNV) encephalitis survivors have cognitive sequelae, particularly impaired memory. Autopsy studies reveal that WNV targets hippocampal neurons.
A multi-institutional team used a mouse model of WNV encephalitis that is very similar to human disease to investigate the mechanism of this cognitive deficit. They demonstrated that WNV infection of neurons triggers activation of the complement cascade; microglial cells then trim presynaptic terminals in response to complement activation. This phenomenon occurs primarily in a region of the hippocampus that is critical for memory. Neuronal death does not occur during pruning of these synapses. In mice that are engineered to have few microglia, and in mice engineered …