Parvovirus B19 Infection and its Association to Autoimmune Disease

Severin, Marianne; Shoenfeld, Yehuda

doi:10.1016/b978-044451271-0.50015-6

Cited by 3 publications

(4 citation statements)

References 47 publications

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“…The parvovirus is at the focus of many dermatologic and rheumatologic disease-related studies previously attributed to unknown factors. [11][12][13][14][15][16][17][18][19][20][21] Initially, B19 was identified as the causative agent of erythema infectiosum (erythrovirus), a common childhood rash found in outbreaks among schoolchildren during the winter and spring months, later called Fifth disease or slapped cheek disease. [22][23][24][25] Since then, B19 has been shown to be the causative agent of many diseases, some of them classified as autoimmune in origin, including arthropathy, transient aplastic crisis, persistent anemia, and hydrops fetalis (Table 1).…”

Section: Introductionmentioning

confidence: 99%

Clinical and Molecular Evidence for Association of SLE with parvovirus B19

Pavlović

Kats

Cavallo

et al. 2010

Lupus

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In addition to genetic and environmental factors, viruses have been suspected as causes and/or contributors to human autoimmune diseases, although direct evidence for the association is generally lacking. Parvovirus B19, the cause of Fifth disease in childhood, and possible trigger in the spectrum of autoimmune diseases in adults, has emerged as one of the central viral candidates within the last few years. In this article we propose a possible model for parvovirus B19 association with systemic lupus erythematosus (SLE). The basis for our model is the secretion of hydrolyzing anti-ssDNA autoantibodies in 30-70% of cases with SLE, which in turn can either hydrolyze viral B19 ssDNA in blood and other fluids, or intranuclear, replicated viral ssDNA after re-activation and translocation of the virus into the nucleus of the host permissive cells. Both mechanisms contribute to perpetuation and maintenance of a 'vicious cycle' with concomitant flares in SLE, and involve inevitable TLR9 sensitization and genetic switch for anti-ssDNA autoantibody production from activated B cells in individuals prone to triggering. This model strongly suggests a major potential impact upon early prevention (vaccination) and targeted therapy of this subclass within the SLE spectrum of diseases. Incorporated in this new concept is an innovative idea for developing the tool for more precise (individualized) diagnosis, prevention, and therapy.

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Section: Introductionmentioning

confidence: 99%

Clinical and Molecular Evidence for Association of SLE with parvovirus B19

Pavlović

Kats

Cavallo

et al. 2010

Lupus

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“…Several similarities exist between RA and Parvo B19 infection: Both states are characterized by a chronic course, morning stiffness, joint deformation and destruction, rheumatoid nodules, as well as by the induction of rheumatoid factor (RF) and of cytokines such as interleukin-6 (IL-6) and transforming growth factor-α (TGF-α). Cases have been reported of RA development after acute Parvo B19 infection and of persistence of B19 RNA and of the VP-1 antigen in the synovial tissue of RA patients [7]. In a study on bone marrow samples from RA patients, 26% were positive for parvovirus B19, as compared to 4% in an historical control group of bone marrow [8].…”

Section: Clinical Associations With Infectionsmentioning

confidence: 99%

“…Another notable association is the development of SLE in patients with HCV and Parvo B19 infection [7]. Attempts to associate parvovirus B19 to SLE have been frustrated [53]; however, acute infections with parvovirus 19 has been associated with disease flare-up [54,55].…”

Section: Clinical Associations With Infectionsmentioning

confidence: 99%

Infections and Autoimmunity: A Panorama

Pordeus

Szyper‐Kravitz

Levy

et al. 2008

Clinic Rev Allerg Immunol

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For more than 2,000 years, it was thought that malignant spirits caused diseases. By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the "germ theory," which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein-Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called 'old friends' (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.

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“…Parvovirus B19 induces aplastic anemia via recruitment of autoreactivity against hematopoietic cells. 18 Similarities between peptide sequences of the infectious agent and of self-antigens lead to the concept that the highly specific T cell recognition fails to distinguish between the infectious agent and self, the T cell thus becoming a victim of molecular mimicry, that is, T cell receptor cross-reactivity involving peptides from an infectious agent and a self-antigen. 19 This is even more important, because autoantibodies present autoantigens to autoaggressive T cells in the form of immune complexes, 20 and consequently may trigger or enhance autoimmune disease.…”

Section: Autoimmune Histo-blood Group Antigensmentioning

confidence: 99%

Histo‐Blood Group Antigens as Allo‐ and Autoantigens

Nydegger

Tevaearai

Berdat

et al. 2005

Annals of the New York Academy of Sciences

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The science of blood groups has made giant steps forward during the last decade. Blood-group typing of red blood cells (RBCs) is performed on more than 15 million samples per year in Europe, today much less often for forensic reasons than for clinical purposes such as transfusion and organ transplantation. Specific monoclonal antibodies are used with interpretation on the basis of RBC agglutination patterns, and mass genotyping may well be on its way to becoming a routine procedure. The discovery that most blood group systems, whose antigens are by definition found on RBCs, are also expressed in multiple other tissues has sparked the interest of transplantation medicine in immunohematology beyond the HLA system. The one and only "histo-blood group" (HBG) system that is routinely considered in transplantation medicine is ABO, because ABO antigen-incompatible donor/recipient constellations are preferably avoided. However, other HBG systems may also play a role, thus far underestimated. This paper is an up-to-date analysis of the importance of HBG systems in the alloimmunity of transplantation and autoimmune events, such as hemolytic anemia.

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Parvovirus B19 Infection and its Association to Autoimmune Disease

Cited by 3 publications

References 47 publications

Clinical and Molecular Evidence for Association of SLE with parvovirus B19

Clinical and Molecular Evidence for Association of SLE with parvovirus B19

Infections and Autoimmunity: A Panorama

Histo‐Blood Group Antigens as Allo‐ and Autoantigens

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