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Molecular epidemiology characterization of the urinary excretion of polyomavirus in healthy individuals from Portugal--a Southern European population.

The human polyomaviruses--BKV and JCV--are members of Polyomaviridae family and after primary infections they persist as latent infection especially in the kidneys. BKV reactivation is mainly related to urinary tract diseases and JCV reactivation can induce the disease progressive multifocal leukoencephalopathy. The aim of our study was to characterize the excretion of polyomaviruses in urine samples of healthy individuals from a Portuguese population. We analyzed 498 DNA samples using PCR-RFLP, the sequence amplified consisted in 176 or 173 bp within the antigen T region. Our results indicate

Isolation of a monoclonal antibody that recognizes the origin binding domain of JCV, but not SV40, large T-antigen.

Within immunocompromised populations, the JC polyomavirus is the cause of the often-fatal disease Progressive Multifocal Leukoencephalopathy (PML). JC virus encodes a protein, termed T-antigen (T-ag), which is essential for its replication and pathogenicity. Previous studies of JCV T-ag have, in general, used antibodies raised against SV40 T-ag. Unfortunately, SV40 T-ag is also detected in humans and therefore there have been concerns about cross-reactivity. To address this issue, we have isolated a monoclonal antibody that binds to the JCV, but not the SV40, T-ag origin-binding domain (OBD). …

John Cunningham Virus and Colorectal Carcinogenesis: Current Evidence, Molecular Mechanisms, and Unresolved Controversies.

Colorectal cancer (CRC) remains a leading cause of cancer-related death worldwide, prompting ongoing research into infectious agents that may contribute to colorectal carcinogenesis. Among candidate oncogenic viruses, JC polyomavirus (JCPyV), a ubiquitous human polyomavirus, has attracted considerable attention due to its potential involvement in tumour initiation and progression. Although several studies have reported the presence of JCPyV viral DNA, transcripts, and proteins in colorectal adenomas and carcinomas, the prevalence and clinical significance of these findings vary considerably ac

Fifty Years of JC Polyomavirus: A Brief Overview and Remaining Questions.

In the fifty years since the discovery of JC polyomavirus (JCPyV), the body of research representing our collective knowledge on this virus has grown substantially. As the causative agent of progressive multifocal leukoencephalopathy (PML), an often fatal central nervous system disease, JCPyV remains enigmatic in its ability to live a dual lifestyle. In most individuals, JCPyV reproduces benignly in renal tissues, but in a subset of immunocompromised individuals, JCPyV undergoes rearrangement and begins lytic infection of the central nervous system, subsequently becoming highly debilitating-an

Inflammatory infratentorial progressive multifocal leukoencephalopathy in a patient with rheumatoid arthritis.

An 84-year-old man with rheumatoid arthritis (RA) treated with methotrexate, developed progressive confusion and cerebellar symptoms, and died approximately 2 months later. Neuropathological examination revealed progressive multifocal leukoencephalopathy (PML) involving the cerebellum and brainstem. The affected tissues displayed intense infiltrations by CD8+ T-cells and microglia. JC virus was localized in oligodendroglia and cerebellar granule cells. This case illustrates unusual localization of inflammatory PML in a patient with RA treated with methotrexate.

Progressive multifocal leukoencephalopathy as first manifestation of sarcoidosis.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating neurologic disorder caused by a polyomavirus, called JC virus. PML affects mainly immunocompromised hosts. We report a case of PML as first manifestation of sarcoidosis in a previously healthy man. Treatment with cidofovir, resulted in a neurological and radiological stabilization. To our knowledge the association of PML and sarcoidosis without previous immunosuppressive treatment has only been described in a few cases, none of them were treated with cidofovir.

AIDS: neurological opportunist infections in central London.

Twenty six (41%) of 64 central London cases of AIDS with nervous system involvement during the course of the illness had neurological opportunist infection. Cytomegalovirus and Toxoplasma gondii were the commonest agents in 22 cases with central nervous system (CNS) infection. Eight cases had herpes zoster radiculopathy. Other infections included those caused by Cryptococcus neoformans, Mycobacterium tuberculosis and papova JC virus. Prognosis was generally poor, irrespective of whether the opportunist infection was treatable.

Доклад по делу: Нейрофильная световая цепочка в последующей деятельности в связи с прогрессивной многофукальной лейкоэнцефалопатией у пациента с множественным склерозом, который лечится окролисумабом.

Прогрессивная многофукальная лейкоэнцефалапатия (ПМЛ) является результатом возобновления вируса Джона Каннингема (JC) и представляет собой редкое осложнение наркотерапии против CD20. Нейрофильтрационные световые цепи все чаще служат в качестве маркера нейроаксональных повреждений при наблюдении за пациентами с множественным склерозом (MS), однако их роль в мониторинге и обнаружении таких процессов, как PML, еще не определена. Мы сообщаем о случае пациента с MS, который лечился острелизумабом и развивал PML. Результаты: Уровень световой цепи серой нейрофильтрации (SNFL) был повышен при диагност

Совпадение в аннотации оригинала
Progressive multifocal leukoencephalopathy (PML) results from the reactivation of John Cunningham virus JC virus and is a rare complication of anti-CD20 drug therapy. Neurofilament light chains increasingly serve as a marker of neuroaxonal damage in the follow-up of patients with multiple sclerosis (MS), but its role in the monitoring and detection of proces…

Head tremor and progressive multifocal leukoencephalopathy in AIDS patients: report of two cases.

Progressive multifocal leukoencephalopathy (PML) is caused by replication of JC virus in oligodendrocytes of immunocompromised patients. Common manifestations are focal motor and sensory deficits, gait abnormalities, speech and language disturbances, cognitive disorders, headache, and visual impairment. Although the occurrence of movement disorders is rare in PML, bradykinesia, rigidity, dystonia, myoclonic jerks and myoclonic ataxia have been described. Head tremor associated with PML has not been previously reported. We report two cases of PML in whom head tremor was present.

Elevation of myoinositol is associated with disease containment in progressive multifocal leukoencephalopathy.

MRI, 1H-MR spectroscopy, immunologic, and virologic studies were performed in search of prognostic factors of disease evolution in patients with progressive multifocal leukoencephalopathy (PML). Acute lesions of PML survivors showed twofold higher standard score of the ratio of myoinositol (a glial marker) to creatine compared with lesions in patients whose disease progressed. Concomitantly, JC virus-specific cytotoxic T lymphocytes were only detected in the blood of PML survivors. These results suggest that inflammation limits disease progression.

Construction and characterization of hybrid polyomavirus genomes.

Several studies have suggested that certain unique features of the JC virus (JCV) regulatory region are responsible for the restricted lytic and transforming activities of this virus in vitro. To pursue this possibility, we have constructed hybrid polyomavirus genomes by exchanging the regulatory sequences of JCV, BK virus (BKV), and simian virus 40 (SV40). The host range of JCV was not expanded by the substitution of the BKV or SV40 regulatory signals; such hybrids were nonviable even in primary human fetal glial cells, the sole permissive cell for JCV. However, chimeric DNAs containing JCV r…

[Progressive multifocal leukoencephalopathy in HIV-positive individuals].

The article discusses the historical aspect and modern ideas about the etiology and pathogenesis of progressive multifocal leukoencephalopathy in patients with HIV infection. An analysis and synthesis of literature data on the clinical presentation of this pathology was carried out. The possibilities and limitations of laboratory and instrumental diagnostic methods, including neuroimaging methods, are discussed in detail. The pathomorphological signs of the disease in HIV-positive individuals are covered.

Bridging the Gap: Immunotherapy in Progressive Multifocal Leukoencephalopathy: A New Hope?

Progressive multifocal leukoencephalopathy (PML) is a severe infection of the CNS occurring in immunocompromised individuals in which large demyelinating lesions are induced by polyomavirus JC (JCV). In the absence of effective antiviral treatment, control of the infection relies on restoring anti-JCV immunity. Thus, particularly in long-standing immunocompromising conditions such as organ transplantation, lymphoproliferative disorders, or idiopathic lymphopenia, new strategies to boost anti-JCV immune responses are needed. Here, we report the case of a patient developing PML in the context of

Sequential treatment of progressive multifocal leukoencephalopathy with intravenous immunoglobulins and pembrolizumab.

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease of the CNS caused by the human polyomavirus 2 (JCV). PML predominantly occurs in immunocompromised patients. To date, no specific antiviral treatment exists, leaving only restoration of the immune system as possible treatment. In 2019, the monoclonal antibody pembrolizumab was reported as a potential treatment option in PML in a case series. Following case reports could not thoroughly confirm a positive outcome. Pembrolizumab targets the inhibitory programmed cell death protein 1 (PD-1) receptor on lymphocytes and

Treatment of Progressive Multifocal Leukoencephalopathy With Mirtazapine.

BACKGROUND AND OBJECTIVES: Progressive multifocal leukoencephalopathy (PML) is a rare, JC-virus-mediated, demyelinating disease with a high mortality rate. As no recommended treatment exists, mirtazapine, a potential blocker of virus entry into cells, has been empirically used. METHODS: We analysed existing data on mirtazapine's efficacy to treat PML by systematically reviewing the literature since 2005, when it was first used. RESULTS: Searches in PubMed, EBSCO, SCOPUS and Google Scholar between January 2005 and December 2015, identified five cohort studies and 74 case reports. No statistic

Progressive multifocal leukoencephalopathy complicating Waldenström's macroglobulinaemia.

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating neurological disorder caused by JC virus. Immunocompromised patients such as those with chronic lymphocytic leukemia, AIDS and following organ transplantation are at increased risk. We report a patient with PML complicating longstanding Waldenström's macroglobulinaemia. Although PML is a rare occurrence, the newer highly immunosuppressive treatment approaches for patients with lymphoproliferative disorders necessitate a high index of clinical suspicion. The diagnosis should be considered in patients with compatible clinic…

Papovavirus detection by electron microscopy in the brain of an elderly patient without overt progressive multifocal leukoencephalopathy.

Virions resembling papovavirus were demonstrated in glial cells in the brain of an aged patient without overt progressive multifocal leukoen … ral subunits of papovavirus capsids. This case provides further evidence that papovavirus, possibly JC virus, may be reactivated in the brains of aged patients who are not in an immunocompromised state.

Meningoencephalitis and demyelination are pathologic manifestations of primary polyomavirus infection in immunosuppressed rhesus monkeys.

The human polyomavirus JC (JCV) is the etiologic agent of progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the CNS that occurs in immunosuppressed individuals. Because polyomavirus-induced CNS pathology usually occurs as a result of the reactivation of latent virus, little is known about the disease manifestations of a primary polyomavirus-induced disease in man. To model such a primary infection, SV40-negative rhesus monkeys were immunosuppressed by infection with the virus SHIV-89.6P and then superinfected with the polyomavirus SV40. The animals developed CNS path