We further noted that in the JCV-infected human glial chimeras, that hGPCs and astrocytes were infected more rapidly than were oligodendrocytes, and viral replication was noted primarily in astrocytes and hGPCs rather than in oligodendrocytes, which instead exhibited viral T antigen-associated apoptotic death. By establishing human glial chimeras in wild-type rather than hypomyelinated hosts - which produced mice colonized with human astrocytes and GPCs but not oligodendrocytes - we then established that human astroglia were sufficient for JCV spread, and that astrocytes, rather than oligodendrocytes, were the principal targets for, and reservoir of, infection in vivo (Kondo et al. 2014).
