JC virus identified in a patient with persistent and severe West Nile virus disease

Zuckerman, Neta S.; Indenbaum, Victoria; Milo, Ron; Mendelson, Ella; Lustig, Yaniv

doi:10.1007/s13365-019-00744-z

Cited by 1 publication

(1 citation statement)

References 14 publications

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“…Yet, development and behavior of CD8 T RM are dictated by their tissue environment; thus, the factors that guide T RM evolution cannot readily be extrapolated between different tissues and pathogens. Extensive work has described the contributions of myeloid cells, T cells, and glia in virus-associated demyelination mouse MS models and West Nile Virus, lymphocytic choriomeningitis virus, Zika virus, and vesicular stomatitis virus CNS infections [131][132][133][134][135][136]. Far less is known about the immunity and inflammatory responses to persistent viral encephalitis, with most studies using mouse models of latent herpesvirus (human simplex virus and murine cytomegalovirus) CNS infection [137,138].…”

Section: Brain-resident Memory (Bt Rm ) Cd8 T Cells-balancing Protect...mentioning

confidence: 99%

Understanding polyomavirus CNS disease – a perspective from mouse models

2021

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JC polyomavirus (JCPyV), a ubiquitous human pathogen, causes several devastating brain diseases in immune compromised individuals. The most notable of these JCPyV-associated CNS diseases is the frequently fatal demyelinating brain disease progressive multifocal leukoencephalopathy (PML).PML, an AIDS-defining disease in the pre-cART epoch, has emerged as a life-threatening complication in patients receiving immunomodulatory agents for autoimmune and inflammatory disorders and treatment for certain hematological malignancies. Among the rapidly expanding list of PML-associated biologics, natalizumab (Tysabri ® ) has the highest incidence and is an ominous sequela for multiple sclerosis (MS) patients who otherwise benefit from dramatic reductions in relapses using this immunomodulatory agent. Drug withdrawal, the only therapeutic option for PML, is often complicated by a high-mortality cerebral inflammatory reaction. No anti-JCPyV agents are Accepted ArticleThis article is protected by copyright. All rights reserved available. Lack of a tractable animal model of polyomavirus-induced central nervous system (CNS) disease is an acknowledged bottleneck to elucidating PML pathogenesis, immunological mechanisms that control JCPyV, in vivo evaluation of agents that inhibit polyomavirus replication in tissue culture and uncovering early events that presage JCPyV-associated neuropathology. The natural virus-host mouse polyomavirus (MuPyV) model has recently been developed to explore mechanisms of polyomavirus-associated CNS disease. In this review, we will cover the benefits of using the MuPyV model to answer fundamental questions about innate and adaptive immune control of JCPyV, the impact of immunomodulation on JCPyV pathogenesis, and how this MuPyV CNS infection model will help improve criteria for identifying patients at risk for JCPyV-associated CNS diseases before development of irreversible lesions.

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