Rearrangement of the JC virus regulatory region sequence in the bone marrow of a patient with rheumatoid arthritis and progressive multifocal leukoencephalopathy

Marzocchetti, Angela; Wüthrich, Christian; Tan, Chen; Tompkins, Troy; Bernal-Cano, Francisco; Bhargava, Parul; Ropper, Allan H.; Koralnik, Igor J.

doi:10.1080/13550280802356837

Cited by 47 publications

(53 citation statements)

References 17 publications

(12 reference statements)

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“…Archetype is rarely associated with PML tissue (554). The consistent isolation of tandem repeat-like NCCR sequences including the 98-bp tandem repeat in tissues obtained from PML patients strongly suggests the importance of this structure in viral pathogenesis (154,214,317,322,510). The prototype and prototype-like sequence variants are generally found in PML tissue, while kidney-and urine-derived NCCR sequences are normally homologous to archetype.…”

Section: Analysis Of the Viral Genomementioning

confidence: 99%

“…Since it has been posited that the viral genome recombines and/or rearranges during DNA replication, an attractive model is that these events occur in B cells, which can undergo V(D)J recombination. This hypothesis is bolstered by the observation that diverse viral NCCRs, including archetype-like and prototype-like NCCRs, have been found in the blood and bone marrow (214,322,484).…”

Section: Potential Viral Dna Recombination and Replication In Cells Omentioning

confidence: 99%

“…Further inquiry led to the observation that cells of the immune system, including hematopoietic progenitor cells and B lymphocytes, as well as tonsillar stromal cells and Schwan cells are susceptible to JC virus (19,341,342,345). Additionally, it was found that JCV may remain latent in immune cells of the bone marrow (198,201,322,484).…”

Section: Cell Type Specificity Of Jcvmentioning

confidence: 99%

“…Additional support for the role of the repeat NCCR structure in pathogenesis has been the identification of prototype-like sequences in cells suspected of harboring latent virus, including lymphocytes isolated from peripheral blood (121,341,444,494) and the bone marrow (201,322,484). Interestingly, the B cell development from CD34 ϩ progenitor to mature plasma cells capable of secreting IgG requires the expression of genes that support and carry out recombination (467).…”

Section: Analysis Of the Viral Genomementioning

confidence: 99%

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Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

et al. 2012

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SUMMARY Progressive multifocal leukoencephalopathy (PML) is a debilitating and frequently fatal central nervous system (CNS) demyelinating disease caused by JC virus (JCV), for which there is currently no effective treatment. Lytic infection of oligodendrocytes in the brain leads to their eventual destruction and progressive demyelination, resulting in multiple foci of lesions in the white matter of the brain. Before the mid-1980s, PML was a relatively rare disease, reported to occur primarily in those with underlying neoplastic conditions affecting immune function and, more rarely, in allograft recipients receiving immunosuppressive drugs. However, with the onset of the AIDS pandemic, the incidence of PML has increased dramatically. Approximately 3 to 5% of HIV-infected individuals will develop PML, which is classified as an AIDS-defining illness. In addition, the recent advent of humanized monoclonal antibody therapy for the treatment of autoimmune inflammatory diseases such as multiple sclerosis (MS) and Crohn's disease has also led to an increased risk of PML as a side effect of immunotherapy. Thus, the study of JCV and the elucidation of the underlying causes of PML are important and active areas of research that may lead to new insights into immune function and host antiviral defense, as well as to potential new therapies.

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Section: Analysis Of the Viral Genomementioning

confidence: 99%

Section: Potential Viral Dna Recombination and Replication In Cells Omentioning

confidence: 99%

Section: Cell Type Specificity Of Jcvmentioning

confidence: 99%

Section: Analysis Of the Viral Genomementioning

confidence: 99%

See 2 more Smart Citations

Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

et al. 2012

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“…44 This hypothesis fits with the observation of the presence of both archetype JC virus and that with a rearranged regulatory region in the bone marrow. 45 Genetic rearrangement in the promoter region may not be the only alteration that increases the neuropathogenecity of the virus. Amino acid substitutions in the VP1 capsid protein of the virus may also play a role in virulence.…”

Section: Aids and Pmlmentioning

confidence: 99%

Monoclonal antibodies and progressive multifocal leukoencephalopathy

Berger

Houff

Major

2009

mAbs

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Incidence and risk factors for Progressive Multifocal Leukoencephalopathy among patients with selected rheumatic diseases

Bharat¹,

Xie²,

Baddley³

et al. 2012

Arthritis Care & Research

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We conducted a large, population-based study to describe the incidence and risk factors for progressive multifocal leukoencephalopathy (PML) among patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), psoriasis (PsO), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), and ankylosing spondylitis (AS) using national inpatient and outpatient administrative data from the entire Center for Medicare and Medicaid Services (CMS) from 2000–2009. Suspected PML cases were identified using hospital discharge diagnosis codes. Risk factors for PML were evaluated using outpatient data >= 6 months prior to PML diagnosis. Among 2,030,578 patients with autoimmune diseases of interest, a total of 53 PML cases were identified (2.6/100,000 patients). Most PML cases had HIV and/or cancer. Nine PML cases had evidence for biologic use prior to PML hospitalization, of which 3 had neither HIV nor malignancy and were exposed to biologics within 12 (rituximab) or 6 months(all other biologics) prior to PML diagnosis. PML occurred at an estimated incidence of 0.2/100,000 patients with autoimmune diseases who did not have HIV or malignancy. PML occurs at a very low incidence among patients with rheumatic diseases but can occur even in the absence of HIV or malignancy.

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Rearrangement of the JC virus regulatory region sequence in the bone marrow of a patient with rheumatoid arthritis and progressive multifocal leukoencephalopathy

Cited by 47 publications

References 17 publications

Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

Monoclonal antibodies and progressive multifocal leukoencephalopathy

Incidence and risk factors for Progressive Multifocal Leukoencephalopathy among patients with selected rheumatic diseases

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