Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects

Rossi, Andrea; Delbue, Serena; Mazziotti, Romina; Valli, Marilena; Borghi, Elisa; Mancuso, Roberta; Calvo, Maria Gaetana; Ferrante, Pasquale

doi:10.1002/jmv.20829

Cited by 50 publications

(43 citation statements)

References 25 publications

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“…This study confirmed previous results that demonstrated how subtype I was predominant in urine samples obtained from patients with bone marrow transplants and hemorrhagic cystitis . The epidemiology of JC virus shows that genotype I is the most common JC virus circulating in Europe and the genome detected most frequently in the Italian population [Stoner et al, 2000;Agostini et al, 2001a;Pagani et al, 2003;Rossi et al, 2007]. In these seven patients, the JC genotype IA was detected in co-infected individuals, whereas in patient no.…”

Section: Discussionmentioning

confidence: 85%

Viral infection in bone marrow transplants: Is JC virus involved?

Mischitelli

Fioriti

Anzivino

et al. 2009

Journal of Medical Virology

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Hemorrhagic cystitis is characterized by hematuria due to inflammation of the bladder. In bone marrow transplants, this disease is linked to the infection by human polyomavirus BK, whereas the role of the human polyomavirus JC is unclear. The transcriptional control regions of both viruses contain important cellular transcription factor binding sites that undergo rearrangement process generating suitable variants that could be more active for viral replication and for the onset of hemorrhagic cystitis. In this study urine obtained from seven patients with bone marrow transplant were examined. Polyomavirus genomes were quantified by PCR and viral loads were compared. The transcriptional regions of both viruses were amplified and sequenced to determine the presence of variants. Subtypes of polyomaviruses were determined by amplification and sequencing of the viral protein 1 region. The results showed that four of seven patients were positive for BK DNA, two of seven patients had BK and JC DNA and one of seven had JC DNA. Positive samples were amplified and sequenced successively for transcriptional regions. The viral archetype was always found in both viruses. Finally, typing showed that BK virus subtype I infected patients with BK, whereas JC virus genotype IA and genotype 1B were found in patients infected with JC. The data suggest that new and different approaches are required to improve the morbidity and mortality caused by polyoma-associated hemorrhagic cystitis, since it known that BK virus is involved in the onset of hemorrhagic cystitis, whereas the role of JC virus should be investigated further.

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Section: Discussionmentioning

confidence: 85%

Viral infection in bone marrow transplants: Is JC virus involved?

Mischitelli

Fioriti

Anzivino

et al. 2009

Journal of Medical Virology

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“…The genetic structure of RR directly affects viral transcription and replication by change the level of DNA/protein and cofactors binding sites, thus leading to distinct cellular tropism 6 . The urinary shedding of JCV with archetype structure is frequent among healthy and immunocompromised individuals 7,8,9,10 , but rearranged forms with deletions, insertions and duplications are usually found in viruses from blood and brain of patients with PML 11,12 . Much less frequently, the rearranged form of JCV can be found in the urine of patients experiencing asymptomatic reactivation 13 .…”

Section: A Short Background Of Pmlmentioning

confidence: 99%

Natalizumab treatment for multiple sclerosis: updates and considerations for safer treatment in JCV positive patients

Nali

Moraes

Fink

et al. 2014

Arq. Neuro-Psiquiatr.

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Natalizumab is currently one of the best options for treatment of patients with Multiple Sclerosis who have failed traditional prior therapies. However, prolonged use, prior immunosuppressive therapy and anti-JCV antibody status have been associated with increased risk of developing progressive multifocal leukoencephalopathy (PML). The evaluation of these conditions has been used to estimate risks of PML in these patients, and distinct (sometimes extreme) approaches are used to avoid the PML onset. At this time, the biggest issue facing the use of Natalizumab is how to get a balance between the risks and the benefits of the treatment. Hence, strategies for monitor JCV-positive patients undergoing Natalizumab treatment are deeply necessary. To illustrate it, we monitored JCV/DNA in blood and urine of a patient receiving Natalizumab for 12 months. We also bring to discussion the effectiveness of the current methods used for risk evaluation, and the real implications of viral reactivation.Keywords: multiple sclerosis, Natalizumab, JCV, risk factors, progressive multifocal leucoencephalopaty, viruria. RESUMO Natalizumabe é atualmente uma das melhores opções para o tratamento de pacientes com Esclerose Múltipla que não respondem aos tratamentos tradicionais. No entanto, o seu uso prolongado, o uso de terapia imunossupressora prévia e o status sorológico antivírus JC têm sido associados com o risco aumentado de desenvolvimento de Leucoencefalopatia Multifocal Progressiva (LEMP). A avaliação destas condições tem sido utilizada para estimar os riscos do desenvolvimento de LEMP nestes pacientes, e abordagens distintas (por vezes extremas) são empregadas para evitar o aparecimento dessa patologia. Atualmente, o grande desafio está em obter um equilíbrio entre os riscos e os benefícios do tratamento com Natalizumabe. Assim, é crucial desenvolver estratégias para monitorar pacientes portadores do vírus JC sob tratamento com Natalizumabe. A título de ilustração, pesquisamos o vírus no sangue e na urina de um paciente sob tratamento durante 12 meses. Também discutimos a eficácia dos métodos atualmente utilizados para avaliação de riscos e as implicações reais de reativação viral.Palavras-chave: esclerose múltipla, Natalizumabe, vírus JC, leucoencefalopatia multifocal progressiva, viruria. Natalizumab (Tysabri), used for treatment of relapsingremitting multiple sclerosis (MS), is a monoclonal antibody directed to the a4b1 integrin, a subunit of an adhesion molecule expressed on the surface of T lymphocytes. The antibodies act by blocking the migration of T Lymphocytes from blood to the CNS through the blood brain barrier (BBB) and attenuate the inflammatory effects 1 . The AFFIRM study showed that monotherapy with Natalizumab (NTZ) for 2 years decreased the relapse rate by 68% and the disability progression rate by 42% compared with placebo 2 . NTZ is well tolerated and the overall incidence of serious adverse events is low. Although the efficacy of NTZ is up to

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“…JCV excretion in the urine can reach 46% in immunocompetent patients, and the virus usually remains asymptomatic [Pagani et al, 2003;Rossi et al, 2007]. However, reactivation of either virus in immunosuppressed patients can cause several clinical syndromes.…”

Section: Introductionmentioning

confidence: 98%

JC virus DNA in the peripheral blood of renal transplant patients: A 1‐year prospective follow‐up in France

Mengelle¹,

Kamar

Jm³

et al. 2010

Journal of Medical Virology

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There is little information on JC virus (JCV) infection in renal transplant patients. A long-term prospective follow-up study was conducted to assess the incidence of JCV DNA in the blood of 103 adult renal transplant patients enrolled prospectively between 1 January and 31 December 2006. Patients were monitored until April 2008. JCV DNA was quantified by a real-time polymerase chain reaction in whole blood samples collected regularly for at least 1 year post-transplant. JCV was detected in seven patients (6.8%) (31/1,487 whole blood samples) at a median time of 139 days post-transplant. The median JC virus load of the first positive DNA blood sample was 3.4 log(10) copies/ml (1.9-5.7 log(10) copies/ml). Induction therapy were either anti-CD25 monoclonal antibodies (n = 5) or antithymocyte globulins (n = 2). Post-transplant immunosuppressive treatment included steroids with tacrolimus/mycophenolate mofetil (MMF) (n = 2), or ciclosporin/MMF (n = 1), or belatacept/MMF (n = 4). Two patients were also treated with rituximab. All seven patients infected with JCV had other viral infections(s): BK virus (3), Epstein-Barr virus (2), Cytomegalovirus (1) or both BK virus and Epstein-Barr virus (1). Three patients had BKV-associated nephropathy and decoy cells shedding. JCV infection was not associated with acute rejection episodes or nephropathy, regardless of the virus load. No patient developed progressive multifocal leukoencephalopathy during follow-up. Thus the incidence of JCV infection in renal transplant patients was low and not associated with any specific clinical manifestations. JCV replication must still be diagnosed and differentiated from BK virus infection because of its non-aggressive course.

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Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects

Cited by 50 publications

References 25 publications

Viral infection in bone marrow transplants: Is JC virus involved?

Viral infection in bone marrow transplants: Is JC virus involved?

Natalizumab treatment for multiple sclerosis: updates and considerations for safer treatment in JCV positive patients

JC virus DNA in the peripheral blood of renal transplant patients: A 1‐year prospective follow‐up in France

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