ISNV Meeting Supplement |
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Authors: | A Bellizzi C Nardis E Anzivino D M Rodìo D Fioriti M Mischitelli F Chiarini V Pietropaolo |
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Institution: | Department of Health Sciences and Infectious Diseases, Sapienza University, P.le Aldo Moro, 5, 00185 Rome, Italy. |
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Abstract: | Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system caused by the neurotropic
human polyomavirus JC (JCV) lytic infection of oligodendrocytes. PML was first described as a complication of lymphoproliferative
disorders more than 50 years ago and emerged as a major complication of human immunodeficiency virus (HIV) infection in the
1980s. Despite the ubiquity of this virus, PML is rare and always seen in association with underlying immunosuppressive condition,
such as HIV infection, autoimmune diseases, cancer, and organ transplantation. JCV remains quiescent in the kidneys, where
it displays a stable archetypal non-coding control region (NCCR). Conversely, rearranged JCV NCCR, including tandem repeat
patterns found in the brain of PML patients, have been associated with neurovirulence. The specific site and mechanism of
JCV NCCR transformation is unknown. According to one model, during the course of immunosuppression, JCV departs from its latent
state and after entering the brain, productively infects and destroys oligodendrocytes. Although the majority of PML cases
occur in severely immunesuppressed individuals, PML has been increasingly diagnosed in patients treated with biological therapies
such as monoclonal antibodies (mAbs) that modulate immune system functions: in fact, CD4+ and CD8+ T lymphopenia, resulting from this immunomodulatory therapy, are the primary risk factor. Furthermore, JCV reactivation in
nonpermissive cells after treatment with mAbs, such as intestinal epithelial cells in Crohn’s disease patients, in association
with other host tumor-inducing factors, could provide valid information on the role of JCV in several malignancies, such as
colorectal cancer. |
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