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English: FIGURE 6. Physiopathology of JCPyV in the brain. JCPyV enter the brain and infects both phenotypes of glial cells, oligodendrocytes and astrocytes, which results in the activation of the normally dormant protein Survivin, which results in the inhibition of apoptosis, a mechanism to dispose of virally infected cells. In oligodendrocytes, permissive to active infection, this allows time for JCPyV to complete its life cycle, which results in active viral replication in the nuclei, the formation of inclusion bodies, and the lytic destruction of the myelin producing cells end in Progressive Multifocal Leukoencephalopathy. In astrocytes, where the infection is abortive, no viral replication takes, but the viral oncoprotein T-Antigen is expressed. T-Antigen binds and inactivates p53 and pRb, crucial tumor suppressors and can affect important cell cycle regulator pathways, including the Wnt signaling pathway, resulting in the activation of c-Myc. Infection with JCPyV also causes DNA damage, and by binding to IRS-1, the downstream protein if the IGF-1 pathway, it inhibits faithful DNA repair, forcing cells to repair their DNA via non-homologous end-joining, which results in mutations. All these are contributing factors of cellular transformation, which in certain individuals may results in the development of brain tumors.