John Cunningham virus (JCV), the etiological agent of progressive multifocal leukoencephalopathy (PML), is the first human polyomavirus described. After asymptomatic primary infection which occurs in childhood, the virus spreads by the hematogenous route from the primary site of infection to secondary sites including kidneys, lymphoid tissues, peripheral blood leukocytes, and brain to establish latent infection. During immunosuppression the virus undergoes molecular rearrangements that allow it to replicate in glial tissues causing PML. PML occurs in people with underlying immunodeficiency or in individuals being treated with potent immunomodulatory therapies. Although the hypothesis that immune deficiency is a predisposing factor for PML, there are many unsolved issues including the pathogenic mechanisms related to the interaction of JCV infection/reactivation with the host. This is due to the difficulty of propagating the virus in human cell cultures and the absence of an animal model. This review updates current understanding in the context of JCV and human disease.

John Cunningham virus: an overview on biology and disease of the etiological agent of the progressive multifocal leukoencephalopathy / Pietropaolo, V; Prezioso, C; Bagnato, F; Antonelli, G. - In: NEW MICROBIOLOGICA. - ISSN 1121-7138. - ELETTRONICO. - 41:3(2018), pp. 179-186.

John Cunningham virus: an overview on biology and disease of the etiological agent of the progressive multifocal leukoencephalopathy.

Pietropaolo V
Writing – Review & Editing
;
Prezioso C
Writing – Original Draft Preparation
;
BAGNATO, FRANCESCA ROSARIA
Writing – Review & Editing
;
Antonelli G
Writing – Review & Editing
2018

Abstract

John Cunningham virus (JCV), the etiological agent of progressive multifocal leukoencephalopathy (PML), is the first human polyomavirus described. After asymptomatic primary infection which occurs in childhood, the virus spreads by the hematogenous route from the primary site of infection to secondary sites including kidneys, lymphoid tissues, peripheral blood leukocytes, and brain to establish latent infection. During immunosuppression the virus undergoes molecular rearrangements that allow it to replicate in glial tissues causing PML. PML occurs in people with underlying immunodeficiency or in individuals being treated with potent immunomodulatory therapies. Although the hypothesis that immune deficiency is a predisposing factor for PML, there are many unsolved issues including the pathogenic mechanisms related to the interaction of JCV infection/reactivation with the host. This is due to the difficulty of propagating the virus in human cell cultures and the absence of an animal model. This review updates current understanding in the context of JCV and human disease.
2018
jcv; immune response; jcv-associated diseases
01 Pubblicazione su rivista::01a Articolo in rivista
John Cunningham virus: an overview on biology and disease of the etiological agent of the progressive multifocal leukoencephalopathy / Pietropaolo, V; Prezioso, C; Bagnato, F; Antonelli, G. - In: NEW MICROBIOLOGICA. - ISSN 1121-7138. - ELETTRONICO. - 41:3(2018), pp. 179-186.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1104055
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