Abstract
The JC polyomavirus (JCPyV/JCV) is a member of the Polyomaviridae family and is ubiquitious in the general population, infecting 50–80% of individuals globally. A primary infection with JCV usally results in an asymptomatic, persistent infection that establishes latency in the renourinary tract. Reactivation from latency via iatrogenic immununosuppression for allograft transplantation may result in organ pathology and a potential life-threatening neuropathological disease in the form of progressive multifocal leukoencephalopathy (PML). Currently, no treatment exists for PML, a rare complication that occurs after transplantation, with an incidence of 1.24 per 1000 persons a year among solid organ transplant patients. PML is also observed in HIV patients who are immununosuppressed and are not receiving antiretroviral therapy, as well as individuals treated with biologics to suppress chronic inflammatory responses due to multiple sclerosis, Crohn’s disease, non-Hodgkin’s lymphoma, rheumatoid arthritis, and other autoimmune-mediated hematological disorders. Here, we describe the proposed mechanisms of JCV reactivation as it relates to iatrogenic immunosuppression for graft survival and the treatment of proinflammatory disease, such as biologics, proposed trafficking of JCV from the renourinary tract, JCV central nervous system dissemination and the pathology of PML in immunosuppressed patients, and potential novel therapeutics for PML disease.
Highlights
The JC polyomavirus (JCPyV/JCV) is a member of the Polyomaviridae family, genusOrthopolyomavirus, which includes the BK polyomavirus (BKPyV/BKV) [1,2,3]
Transplant recipients who require immunosuppression, have HIV/AIDS, have malignancies, and/or receive routine infusions of biologics to treat autoimmune and inflammatory diseases, such as multiple sclerosis (MS) or Crohn’s disease, should be monitored for abnormal neurological signs and symptoms associated with progressive multifocal leukoencephalopathy (PML)
Transplant patients who require iatrogenic immunosuppression are especially vulnerable to JCV reactivation in the brain, which may expose them to JCV lytic replication in the CNS, demyelination, and the life-threatening
Summary
Orthopolyomavirus, which includes the BK polyomavirus (BKPyV/BKV) [1,2,3]. Both viruses were isolated from patients with the initial JC and BK polyomaviruses, respectively [1,2]. JCV in the brain of immune-compromised individuals may result in a lytic infection of oligodendrocytes, glial cells, and astrocytes [7,8,9,10,11]. PML occurs in 3–5% of HIV-infected individuals with an uncontrolled disease, but HIV therapy has been shown to improve clinical outcomes [6,10,11,18]. This is a significantly higher incidence when compared to patients with other means of immunomodulation therapy. We examine the role of iatrogenic immunosuppression on JCV reaction and the neuropathology that may result post-reactivation
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