Explore chapters and articles related to this topic
Progressive multifocal leukoencephalopathy
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Eric M. L. Williamson, Joseph R. Berger
After the initial clinical and pathological descriptions of PML [1,2,12], evidence of a viral etiology was hypothesized based on electron microscopic studies, which demonstrated papovavirus-like particles in the nuclei of abnormal oligodendrocytes [13,14]. Richardson suspected that the causative agent was a virus based on the cytopathic changes he observed and the fact that the condition occurred as a complication of diseases that weakened the immune system [12]. The etiology was confirmed by viral isolation of a human Polyomavirus (double-stranded DNA-containing virus with icosahedral symmetry) in glial cell cultures from the brain of a patient with PML in 1971 [3]. This papovavirus is capable of hemagglutination of human type O erythrocytes, allowing for the detection of antibodies in patients. In the overwhelming majority of cases of PML suspected on clinical and pathologic grounds in which virologic confirmation has been obtained, JCV is the cause. In only three cases [15,16] has another papovavirus, SV40, been implicated; while a third papovavirus, BK virus, has been proposed but rarely proven to be neuropathogenic. The cases attributed to SV40 have not been well characterized, and in some instances, re-examination of these brain tissues by in situ DNA hybridization has revealed JCV, not SV40 [17].
Oncogenic DNA Viruses
Published in Pimentel Enrique, Oncogenes, 2020
Papillomaviruses are members of the papovavirus group (which include also the polyoma virus and SV40) and have been etiologically related to the appearance of benign epithelial cell proliferative processes of animals and man, including papillomas and warts, which may eventually undergo malignant conversion in certain clinical settings.58 The study of papillomaviruses has been hampered by the lack of a cellular culture system suitable for virus propagation. In spite of this difficulty, these viruses have been studied by molecular cloning, reassociation kinetics of genomic sequences and serological procedures, which permitted the identification of 24 different types of human papillomaviruses (HPV) and 6 types of bovine papillomaviruses (BPV) described until 1984.58
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
This disease, caused by viruses of the polyoma subgroup of papovaviruses, is virtually restricted to immunocompromised patients. Distributed throughout the white matter are multiple small grey foci of demyelination which can coalesce to form large, often cystic, areas. Demyelination is accompanied by large bizarre astrocytes, macrophages, and abnormal oligodendrocytes, the large nuclei of which contain inclusion bodies consisting of pseudocrystalline arrays of virions.
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].