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Order Sepolyvirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The order Sepolyvirales currently involves the sole family Polyomaviridae, 6 genera, and 117 species altogether. The two genera Alphapolyomavirus and Betapolyomavirus are the most populated and well studied, while five polyomavirus species still remain genera-independent. As summarized by the official ICTV reports (Norkin et al. 2012; Moens et al. 2017), the members of the Polyomaviridae family infect mammals, birds, and fish and may cause different forms of neoplasia, while each family member has a restricted host range. Thus, Merkel cell polyomavirus (MCPyV) and raccoon polyomavirus (RacPyV) are associated with cancer in their host. Other members are human and veterinary pathogens causing symptomatic infection in their natural host, whereas the clinical manifestations are observed primarily in immunocompromised patients (Moens et al. 2017).
Cancer-Causing Viruses
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Satya P. Gupta, Vertika Gautam
Polyomaviruses belong to Polyomaviridae family, which is a group of nonenveloped, small, double-stranded DNA viruses. They are potentially oncogenic, and the first polyomavirus, known as mouse polyomavirus (Gross 1953; Stewart et al. 1958), is one of the most aggressive oncogenic viruses. It causes tumors in almost every tissue of susceptible mouse strains (Eddy 1969; Gross 1983). The name polyoma refers to the ability of viruses to produce multiple (poly-) tumors (-oma). Polyomaviruses have approximately 5000 base pairs, a circular genome and icosahedral shape, and do not have a lipoprotein envelope.
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].
Prevention of viral infections in solid organ transplant recipients in the era of COVID-19: a narrative review
Published in Expert Review of Anti-infective Therapy, 2022
Paraskevas Filippidis, Julien Vionnet, Oriol Manuel, Matteo Mombelli
BKV is a DNA virus of the Polyomaviridae family that establishes lifelong latency in the reno-urinary tract. Up to 90% of adult individuals in general population are seropositive [195]. BKV almost exclusively affects immunocompromised patients and it is responsible for most cases of polyomavirus-associated nephropathy after kidney transplantation [196] and polyomavirus-associated hemorrhagic cystitis after allogeneic hematopoietic cell transplantation [197]. In contrast, clinically significant disease in non-renal SOT recipients remains exceptional [198]. No pharmacological agent has demonstrated a clear clinical beneficial antiviral effect on BKV, including cidofovir, brincidofovir, leflunomide, and fluoroquinolones [199,200]. Hence, a preemptive approach with routine monitoring of BKV viremia and reduction of immunosuppression remains the cornerstone for the prevention of polyomavirus-associated nephropathy [198]. Current recommendations suggest monitoring for BKV viremia on a monthly basis until month 9 and then every 3 months until 2 years post-transplant, or in case of unexplained post-transplant nephropathy [198].