Parvovirus B19 infection and autoimmune disease

Lehmann, H; Landenberg, Philipp von; Modrow, Susanne

doi:10.1016/s1568-9972(03)00014-4

Cited by 143 publications

(104 citation statements)

References 37 publications

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“…VP1u has been shown to generate the production of anti-phospholipid antibodies and anti-phospholipid syndromelike autoimmunity via molecular mimicry (36,37). The PLA 2 activity of VP1u is also suspected of contributing to inflammatory processes induced by the production of potent eicosanoid lipid mediators (22). All of these immunological features contrast with our recent findings indicating that the most N-terminal part of VP1u is internal and that the capsids are enzymatically inactive (30).…”

Section: Discussioncontrasting

confidence: 65%

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Interaction of Parvovirus B19 with Human Erythrocytes Alters Virus Structure and Cell Membrane Integrity

Bönsch

Kempf

Ros

2008

J Virol

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The unique region of the capsid protein VP1 (VP1u) of B19 virus (B19V) elicits a dominant immune response and has a phospholipase A 2 (PLA 2 ) activity required for the infection. Despite these properties, we have observed that the VP1u-PLA 2 motif occupies an internal position in the capsid. However, brief exposure to increasing temperatures induced a progressive accessibility of the PLA 2 motif as well as a proportional increase of the PLA 2 activity. Similarly, upon binding on human red blood cells (RBCs), a proportion of the capsids externalized the VP1u-PLA 2 motif. Incubation of B19V with RBCs from 17 healthy donors resulted in extensive virus attachment ranging between 3,000 and 30,000 virions per cell. B19V empty capsids represent an important fraction of the viral particles circulating in the blood (30 to 40%) and bind to RBCs in the same way as full capsids. The extensive B19V binding to RBCs did not cause direct hemolysis but an increased osmotic fragility of the cells by a mechanism involving the PLA 2 activity of the exposed VP1u. Analysis of a blood sample from an individual with a recent B19V infection revealed that, at this particular moment of the infection, the virions circulating in the blood were mostly associated to the RBC fraction. However, the RBC-bound B19V was not able to infect susceptible cells. These observations indicate that RBCs play a significant role during B19V infection by triggering the exposure of the immunodominant VP1u including its PLA 2 constituent. On the other hand, the early exposure of VP1u might facilitate viral internalization and/or uncoating in target cells.

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Section: Discussioncontrasting

confidence: 65%

“…Apart from its immunodominant role, VP1u harbors a phospholipase A 2 (PLA 2 ) motif (13), which is required for the infection (14,18,44). Growing evidence indicates that VP1u also plays a central role in the induction of autoimmune reactions and inflammatory processes (22,36,37,41) by mechanisms still not well understood.…”

mentioning

confidence: 99%

Interaction of Parvovirus B19 with Human Erythrocytes Alters Virus Structure and Cell Membrane Integrity

Bönsch

Kempf

Ros

2008

J Virol

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“…Among the few viruses that are suspected to play a role, parvovirus B19 likely represents the most compelling candidate (12). B19 has been associated with a variety of autoimmune diseases (147), and several publications have reported the cooccurrence of acute B19 infection and WG (12,148,149). Moreover, acute B19 infection may trigger production of C-or P-ANCA and PR3-or MPO-ANCA, and these autoantibodies disappear, at least in some instances, once the infection has subsided (147,150,151); however, none of these cases of ANCApositive B19 infection presented with clinical signs suggestive of systemic vasculitis (147,150,151), and larger serologic (152,153) or molecular investigations (153,154) have not supported the relationship between B19 infection and ANCA-associated vasculitis.…”

Section: Viral Infectionsmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

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The first description of what is now known as antineutrophil cytoplasmic autoantibody-associated necrotizing vasculitis appeared more than 140 yr ago. Since then, many aspects of the pathogenic pathway have been elucidated, indicating the involvement of antineutrophil cytoplasmic autoantibodies, but why antineutrophil cytoplasmic autoantibodies are produced in the first place remains unknown. Over the years, many hypotheses have emerged addressing the etiology of antineutrophil cytoplasmic antibody production, but no exclusive factor or set of factors can so far be held responsible. Herein is reviewed the most influential hypotheses regarding the causes of antineutrophil cytoplasmic antibody-associated vasculitis with the aim of placing in an epidemiologic background the different hypotheses that are centered on environmental and genetic influences.Clin J Am Soc Nephrol 3: 237-252, 2008237-252, . doi: 10.2215 A ntineutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing vasculitis was probably first described in 1866 by Kussmaul and Maier (1) as "polyarteritis nodosa." It was not until the early 1930s when the first case of what was later named Wegener's granulomatosis (WG) was described (2). The disease was named after Friedrich Wegener, who described it as an entity in 1939 (3). In 1985, antibodies associated with the disease were detected and later became known as ANCA (4). WG is a systemic autoimmune disease that can cause damage in various organs. Later, microscopic polyangiitis (MPA) was distinguished as a separate ANCA-associated vasculitis. The disease-or its immunosuppressive treatment-can cause high levels of morbidity and death, especially in patients with renal involvement. Animal experiments have shown that ANCA directed against myeloperoxidase (MPO) can cause vasculitis that resembles human vasculitic disease (5,6); however, the cause of ANCA production remains unresolved.Theories have been developed to explain how ANCA could interact with neutrophils, along with monocytes and most probably T lymphocytes, to form the lesions that are characteristic of ANCA-associated vasculitis, such as fibrinoid necrosis and granulomas (7). A recent theory of interest has been postulated by Pendergraft et al. (8), stating that an antibody against the complementary peptide of proteinase-3 (PR3) in an idiotypic/anti-idiotypic network is essential to the development of ANCA and to the development of clinical vasculitis, but why and how these ANCA are produced in the first place remains unanswered. Nonetheless, many hypotheses have been developed about the initiating factor for ANCA production. Many factors, either directly or indirectly, have been considered important in the development of ANCA: Silica exposure (9); genetic predisposition (10); bacterial infection by Staphylococcus aureus (11); viral infection by, for instance, parvovirus B19 (12); and thyroid drugs (13) all have been correlated with and held to contribute to the incidence of ANCA-associated vasculitis. Some of these hypotheses are still th...

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“…6 Parvovirus B19 belongs to the Parvoviridae family of small DNA viruses. 7 Infection with parvovirus B19 (B19) is a global concern and the infection rate is similar in the United States, Europe and Asia, with approximately half of 15-year-old adolescents and over 60% of adults being seropositive. 8,9 Parvovirus B19 is a common human pathogen, which has been linked to autoimmune diseases recently.…”

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confidence: 99%

The Relationship Between Parvovirüs B19 and Hashimoto\'s Thyroiditis

Erden¹,

Çıftçı²,

Çınar³

et al. 2013

Turkiye Klinikleri J Med Sci

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98ashimoto's thyroiditis (HT) is the most common and extensively studied organ-specific autoimmune disorder in humans. 1,2 It is characterized by diffuse lymphocytic infiltration of the thyroid gland, elevated levels of the serum antithyroid antibodies (ATA) The chi-square test and unpaired t-test were used for the comparison between the groups. R Re es su ul lt ts s: : Anti-parvo virus IgM antibodies were positive in 6 (11.1%) patients and 3 (5.7%) controls while anti-parvo virus IgG antibodies were present in 14 (25.9%) patients and 8 (22.9 %) controls. There was no significant difference between the patient and control groups in terms of antibody positivity (p=0.409, p=0.478). C Co on nc cl lu us si io on n: : Although the prevalence of antiviral antibodies were higher in patients with HT compared to those in the control group, the difference was not statistically significant. This was attributed to the small number of patients. Nevertheless, this finding may reflect a viral contribution in the pathogenesis of HT.

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Parvovirus B19 infection and autoimmune disease

Cited by 143 publications

References 37 publications

Interaction of Parvovirus B19 with Human Erythrocytes Alters Virus Structure and Cell Membrane Integrity

Interaction of Parvovirus B19 with Human Erythrocytes Alters Virus Structure and Cell Membrane Integrity

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

The Relationship Between Parvovirüs B19 and Hashimoto\'s Thyroiditis

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