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Clinical and Developmental Immunology
Volume 2013, Article ID 839719, 17 pages
Review Article

New Insights on Human Polyomavirus JC and Pathogenesis of Progressive Multifocal Leukoencephalopathy

1Department of Public Health and Infectious Diseases, “Sapienza” University of Rome, P.le Aldo Moro, 5-00185 Rome, Italy
2Department of Public Health and Infectious Diseases, Institute Pasteur, Cenci-Bolognetti Foundation, “Sapienza” University of Rome, P.le Aldo Moro, 5-00185 Rome, Italy
3San Raffaele Pisana Scientific Institute for Research, Hospitalization and Health Care, Via Val Cannuta, 247-00166 Rome, Italy
4Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, 1900 N. 12th Street, Philadelphia, PA 19122, USA

Received 7 January 2013; Accepted 6 March 2013

Academic Editor: Serena Delbue

Copyright © 2013 Anna Bellizzi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


John Cunningham virus (JCV) is a member of the Polyomaviridae family. It was first isolated from the brain of a patient with Hodgkin disease in 1971, and since then the etiological agent of the progressive multifocal leukoencephalopathy (PML) was considered. Until the human immunodeficiency virus (HIV) pandemic, PML was rare: in fact HIV-induced immunodeficiency is the most common predisposing factor accounting for 85% of all instances of PML. This data led to intense research on JCV infection and resulted in better understanding of epidemiology and clinic-pathologic spectrum. Recently, cases of PML have been observed after the introduction of monoclonal antibodies, such as natalizumab, rituximab, efalizumab, and infliximab, in the treatment of autoimmune disease, underlining the important role of host immunity in PML pathogenesis. In this review current understanding of the JCV infection and the new findings relating to the pathogenesis of PML has been comprehensively revised, focusing our attention on the interaction between the cellular and viral molecular pathways implicated in the JCV infection and the modulating role of host immune surveillance in the viral reactivation from a latent state.