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Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
JC virus infection is ubiquitous and usually acquired in childhood, with approximately 70–85% of adults in the United States possessing antibodies to the virus.1,2 PML was once quite rare, but the HIV pandemic has changed the epidemiology dramatically. PML was seen occasionally in patients with hematologic malignancies,3,4 steroid use,5 or the rare patient of advanced age. It has also been reported in presumably immunocompetent individuals. However, PML is currently considered a disease of the immunocompromised, particularly those with AIDS, and patients receiving cytotoxic chemotherapy or other immunosuppressive agents. More than 50% of all deaths from PML occur in HIV-infected individuals, and it is estimated that 1–4% of patients with HIV will develop PML.6
Oncological effects on the central nervous system
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
A number of treatment options are under investigation, including use of antiviral agents to suppress JC virus (e.g. cidofovir, mefloquine) or use of immune response modulators (e.g. interleukin 7), although the prognosis still remains poor (27).
Multiple Sclerosis, Transverse Myelitis, Tropical Spastic Paraparesis, Progressive Multifocal Leukoencephalopathy, Lyme Disease
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Michele Fascelli, Howard B. Goldman
Progressive multifocal leukoencephalopathy (PML) is an infectious demyelinating brain disease caused by JC virus (JCV), which is associated with significant morbidity and mortality in the immunosuppressed (IS) host. Considered a rare opportunistic infection of the CNS, PML has recently been associated with select IS patients with MS, particularly those treated with natalizumab.85
JC polyomavirus: a short review of its biology, its association with progressive multifocal leukoencephalopathy, and the diagnostic value of different methods to manifest its activity or presence
Published in Expert Review of Molecular Diagnostics, 2023
Carla Prezioso, Valeria Pietropaolo, Ugo Moens, Marco Ciotti
In 1958, Åstrom and colleagues described a fatal demyelinating condition affecting multiple foci of the subcortical white matter in two patients suffering from chronic lymphocytic leukemia and one with Hodgkin’s lymphoma and named the disease Progressive Multifocal Leukoencephalopathy (PML) [1]. Patients with PML were rare, and the cause of this disease was an enigma. Because of the presence of inclusion bodies in oligodendrocytes, a viral etiology hypothesis was put forward [2,3]. Electron microscopic observations in the 1960s of PML affected brain tissue confirmed the presence of icosahedral shaped virus particles resembling papovavirus in these intranuclear inclusions [4,5]. Several years later, Padgett and colleagues succeeded in isolating this virus and propagating it in primary fetal glial cells. They named the virus J.C. after the initials of the patient [6] and of ethical considerations the patient’s full name should not be used [7]. JC virus is currently classified as a polyomavirus (PyV) belonging to the Polyomaviridae family, genus Betapolyomavirus, species Betapolyomavirus secuhominis. The International Committee on Taxonomy of Viruses proposed to use the binomial nomenclature JC polyomavirus (abbreviated as JCPyV) or betapolyomavirus secuhominis [8].
Infratentorial onset of progressive multifocal leukoencephalopathy in a patient with systematic lupus erythematosus complicated with lymphoma: a case report
Published in Modern Rheumatology Case Reports, 2021
Mita Sakuraba, Shinji Watanabe, Yasuhiro Nishiyama, Kenta Takahashi, Kazuo Nakamichi, Mikito Suzuki, Takashi Nawata, Kota Komai, Takahisa Gono, Mitsuhiro Takeno, Tadaki Suzuki, Kazumi Kimura, Masataka Kuwana
Progressive multifocal leukoencephalopathy (PML) is a progressive demyelinating disease of the central nervous system (CNS) caused by reactivation of JC virus (JCV) in immunocompromised subjects, including those with acquired immunodeficiency syndrome, cancer, organ transplantation, and autoimmune diseases [1]. Recently, antiretroviral therapy has successfully reduced the incidence of PML in human immunodeficiency virus (HIV)-infected individuals [2]. In contrast, the incidence of PML is increasing in patients with autoimmune diseases treated with potent immunosuppressive therapies [3]. Systemic lupus erythematosus (SLE) is the leading underlying disease of PML and comprises approximately two-thirds of reported cases. The incidence of PML in SLE patients has been estimated to range from 1.0 to 2.4 cases/100,000 person-years [4,5].
How not to discover a drug - integrins
Published in Expert Opinion on Drug Discovery, 2021
While a promising therapy for both MS and Crohn’s there was a serious safety concern with natalizumab. It was associated with reactivation of JC virus infection leading to Progressive Multifocal Leukoencephalopathy (PML) [140] due to lysis of neurons and permanent destruction of the myelin sheath. In patients that are JC virus positive the incidence of PML is 1% with a 25% mortality rate and 30% of survivors will have severe neurological complications [141]. This was to be a major blow for natalizumab. While it was an effective disease-modifying therapy its safety profile was of concern. Although it was not withdrawn from the market it is only prescribed under a risk evaluation and mitigation strategy (REMS). With the advent of newer disease modifying therapies such as fingolimod and dimethyl fumarate it is no longer a frontline treatment. PML is not unique to natalizumab with a number of other immune suppressants associated with PML however, the incidence is much higher with natalizumab.