Establishment of functional B cell memory against parvovirus B19 capsid proteins may be associated with resolution of persistent infection

Corcoran, Amanda; Crowley, Brendan; Dewhurst, C. J.; Pizer, Barry; Doyle, Seán

doi:10.1002/jmv.20513

Cited by 7 publications

(5 citation statements)

References 21 publications

(24 reference statements)

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“…Recently, Corcoran et al. [203] showed persistent infection in a child with acute lymphatic leukaemia despite the treatment with intravenous immunoglobulin. Interestingly, resolution of the infection was associated with the simultaneous strengthening of antigen‐specific B‐cell memory against B19 VP2 and diminution in the memory response against B19 NS1.…”

Section: Immune Responses In B19 Infectionmentioning

confidence: 99%

“…The situation in persistent B19 infection may thus resemble that of HBV infection, and the increased T-cell activity seen after interferon treatment of HBV infection, suggests that a similar approach might prove beneficial also in B19-persistent infection [202]. Recently, Corcoran et al [203] showed persistent infection in a child with acute lymphatic leukaemia despite the treatment with intravenous immunoglobulin. Interestingly, resolution of the infection was associated with the simultaneous strengthening of antigenspecific B-cell memory against B19 VP2 and diminution in the memory response against B19 NS1.…”

Section: Immune Responses In Persistently Infected Individualsmentioning

confidence: 99%

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Clinical aspects of parvovirus B19 infection

Broliden

Tolfvenstam

Norbeck

2006

Journal of Internal Medicine

189

203

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Parvovirus B19 is a significant human pathogen that causes a wide spectrum of clinical complications ranging from mild, self-limiting erythema infectiosum in immunocompetent children to lethal cytopenias in immunocompromised patients and intrauterine foetal death in primary infected pregnant women. The infection may also be persistent and can mimic or trigger autoimmune inflammatory disorders. Another important clinical aspect to consider is the risk of infection through B19-contaminated blood products. Recent advances in diagnosis and pathogenesis, new insights in the cellular immune response and newly discovered genotypes of human parvoviruses form a platform for the development of modern therapeutic and prophylactic alternatives.

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Section: Immune Responses In B19 Infectionmentioning

confidence: 99%

Section: Immune Responses In Persistently Infected Individualsmentioning

confidence: 99%

Clinical aspects of parvovirus B19 infection

Broliden

Tolfvenstam

Norbeck

2006

Journal of Internal Medicine

189

203

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“…Assays based on exploitation of the P antigen receptor of B19, known as receptor-mediated hemagglutination (RHA), have been proposed as a cheap way of screening plasma and apparently detect whole virus, however the assay sensitivity is low when compared to PCR and, more importantly, it has not been assessed in an obstetrics context (Cohen and Bates, 1995;Sato et al, 1995;Wakamatsu et al, 1999). In cases where patients are treated with intravenous immunoglobulin (IVIG) to treat chronic B19 infection, assessment of antigen-specific B cell memory allows one to discriminate IVIG-and individual-derived B19 IgG, which is important in determining the seroconversion status of the individual (Corcoran et al, 2005a).…”

Section: Alternative Detection Methodsmentioning

confidence: 99%

Human Parvovirus B19: Molecular Virology, Clinical Features, Prevalence, Diagnosis and Control

Corcoran¹,

Doyle²

2006

Congenital and Other Related Infectious Diseases of the Newborn

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Parvovirus B19-introductionParvovirus B19 (B19) is an erythrovirus and recent studies have classified B19 as a genotype 1 erythrovirus with genotypes 2 (erythrovirus K71 or A6) and 3 (erythrovirus V9) also present in the human population. B19 is a significant human pathogen which can cause foetal hydrops and foetal death if maternal infection, followed by transplacental QA :1 foetal infection, occurs during pregnancy. The virus is also transmitted by inter-personal contact and potentially via blood product administration. Symptoms of B19 infection include malaise, rash and anthralgia. Significantly, maternal B19 infection during pregnancy can be asymptomatic and so careful monitoring of at-risk pregnancies is recommended. Both antibody-and cell-mediated immunity play an important role in the anti-viral response and effective diagnostic test systems, for both B19 antibody and DNA detection, are now available. B19-induced foetal hydrops can be effectively treated by intrauterine blood transfusion; however, no vaccine is available to prevent infection at present.

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“…Further analyses identified two discrete A + T rich elements within the V1 S107 variable heavy chain promoter were bound by a protein complex later identified to contain Bright (3). Intriguingly, further analyses showed potential Bright-binding motifs in about half of the murine V H promoters, and binding sites were not restricted to specific V region families (30, 31). Similarly, only a subset of human V H promoters had binding sites for Bright (32).…”

Section: Gene Targets For Brightmentioning

confidence: 95%

The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis

et al. 2014

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ARID3a/Bright is a DNA-binding protein that was originally discovered for its ability to increase immunoglobulin transcription in antigen-activated B cells. It interacts with DNA as a dimer through its ARID, or A/T-rich interacting domain. In association with other proteins, ARID3a increased transcription of the immunoglobulin heavy chain and led to improved chromatin accessibility of the heavy chain enhancer. Constitutive expression of ARID3a in B lineage cells resulted in autoantibody production, suggesting its regulation is important. Abnormal ARID3a expression has also been associated with increased proliferative capacity and malignancy. Roles for ARID3a in addition to interactions with the immunoglobulin locus were suggested by transgenic and knockout mouse models. Over-expression of ARID3a resulted in skewing of mature B cell subsets and altered gene expression patterns of follicular B cells, whereas loss of function resulted in loss of B1 lineage B cells and defects in hematopoiesis. More recent studies showed that loss of ARID3a in adult somatic cells promoted developmental plasticity, alterations in gene expression patterns, and lineage fate decisions. Together, these data suggest new regulatory roles for ARID3a. The genes influenced by ARID3a are likely to play pivotal roles in lineage decisions, highlighting the importance of this understudied transcription factor. Keywords: Bright, ARID3a, hematopoietic regulation, B cell development, gene regulationBright (B cell regulator of immunoglobulin heavy chain transcription) is a 70 kDa DNA-binding protein first characterized in the mouse as a component of a protein complex associated with increased transcription of the immunoglobulin heavy chain (IgH) locus in activated B lymphocytes (1-3). Bright, also known as DRIL1, E2FBP1, or ARID3a (the designation for the human ortholog, hereafter referred to as Bright), is a member of the A + T rich interaction domain (ARID) protein family, many of which have been shown recently to have epigenetic regulatory functions [reviewed in ]. These proteins bind to A + T rich DNA sequences and are typically members of larger chromatin modulatory complexes. Bright, and other ARID3 family members, require dimerization for DNA-binding activity and contain an extended DNA-binding domain that confers increased DNA sequence specificity to these proteins compared to other ARID family members (7-9). Although Bright was the first member of this family identified in mammalian cells, its functions have only begun to be elucidated. Previously, Bright expression in adult, mouse, and human cells was thought to be largely restricted to B lymphocyte lineage cells. However, more recently, we and others have shown that Bright plays important regulatory functions in early hematopoiesis. Although Bright expression is restricted in adults, it is more widely expressed in the embryo/fetus and plays important regulatory roles in embryonic stem cell differentiation (10). These data also highlight novel roles for Bright in gene repression. This artic...

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Establishment of functional B cell memory against parvovirus B19 capsid proteins may be associated with resolution of persistent infection

Cited by 7 publications

References 21 publications

Clinical aspects of parvovirus B19 infection

Clinical aspects of parvovirus B19 infection

Human Parvovirus B19: Molecular Virology, Clinical Features, Prevalence, Diagnosis and Control

The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis

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