The human polyomavirus JC virus (JCV) infects greater than 80% of the human population. The JC virus is a small (38-40 nm in diameter) double stranded, circular DNA virus covered by an icosahedral capsid. Infection with JCV is asymptomatic and it occurs in early childhood. After the primary infection, the virus remains in latent state in the kidney, until it's reactivation under immunosuppressive conditions to result in Progressive Multifocal Leukoencephalopathy (PML), a fatal demyelinating disease. 70% of all HIV-1- infected patients will exhibit neurological disorders and between 5 and 8% of all HIV-1-infected patients will develop PML. Similar to other polyomaviruses, JCV can cause tumors when intracerebrally inoculated at high titers into developing rodent. Several reports suggest the association of viruses, especially of the polyomavirus family with different types of human brain tumors. Tumorigenecity of JCV is most likely induced by the viral early gene product T-antigen. T-antigen has the capacity to interact with several tumor suppressor proteins, most notably p53, and functionally inactivate these proteins.