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Checkpoint inhibitors and progressive multifocal leukoencephalopathy: friends of foes?
Author(s) -
Daniele Focosi,
Marco Tuccori,
Fabrizio Maggi
Publication year - 2019
Publication title -
annals of translational medicine
Language(s) - English
Resource type - Journals
eISSN - 2305-5847
pISSN - 2305-5839
DOI - 10.21037/atm.2019.11.07
Subject(s) - progressive multifocal leukoencephalopathy , natalizumab , medicine , rituximab , jc virus , leukoencephalopathy , multiple sclerosis , fingolimod , immunology , virology , antibody , pathology , disease
Progressive multifocal leukoencephalopathy (PML) has evolved in the last decade from a disorder of acquired immune deficiency syndrome (AIDS) patients into a rare but fatal complication of several life-saving therapeutics (ranging from rituximab in non-Hodgkin lymphomas to natalizumab in multiple sclerosis). PML is linked to opportunistic reactivation of the latent human JC polyomavirus (JCV), which leads to emergence of neurotropic strains causing brain demyelination.

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