The role of parvovirus B19 in the pathogenesis of autoimmunity and autoimmune disease

Human parvovirus B19 is a single-stranded DNA virus which preferentially targets the erythroblasts in the bone marrow. B19 infection commonly causes erythema infectiosum, arthralgia, fetal death, transient aplastic crisis in patients with shortened red cell survival, and persistent infection in peop...

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Autores:
Tipo de recurso:
Fecha de publicación:
2016
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/22309
Acceso en línea:
https://doi.org/10.1136/jclinpath-2015-203455
https://repository.urosario.edu.co/handle/10336/22309
Palabra clave:
Angiotensin 1 receptor
Autoantibody
Autoantigen
Cardiolipin
Collagen type 2
Fibrinogen receptor
Glutamate decarboxylase
Glycoprotein iib
Keratin
Myelin basic protein
Phospholipase
Rheumatoid factor
Autoantibody
Autoantigen
Aplastic crisis
Arthralgia
Autoimmune disease
Brachial plexus neuropathy
Cerebellar ataxia
Chronic fatigue syndrome
Cranial nerve paralysis
Cytopenia
Enzyme activity
Erythema infectiosum
Erythrocyte lifespan
Fetus death
Graves disease
Guillain barre syndrome
Heart disease
Hematologic disease
Human
Human parvovirus b19
Immune response
Insulin dependent diabetes mellitus
Myalgia
Myelitis
Myositis
Neurologic disease
Nonhuman
Pathogenesis
Persistent infection
Priority journal
Rash
Review
Rheumatoid arthritis
T lymphocyte
Thyroid disease
Virus transmission
Autoimmune disease
Autoimmunity
Cross reaction
Erythema infectiosum
Human parvovirus b19
Immunology
Molecular mimicry
Virology
Autoantibodies
Autoantigens
Autoimmune diseases
Autoimmunity
Cross reactions
Erythema infectiosum
Humans
Molecular mimicry
human
Parvovirus b19
Rights
License
Abierto (Texto Completo)
Description
Summary:Human parvovirus B19 is a single-stranded DNA virus which preferentially targets the erythroblasts in the bone marrow. B19 infection commonly causes erythema infectiosum, arthralgia, fetal death, transient aplastic crisis in patients with shortened red cell survival, and persistent infection in people who are immunocompromised. Less common clinical manifestations include atypical skin rashes, neurological syndromes, cardiac syndromes, and various cytopenias. B19 infection has also been associated with development of a variety of different autoimmune diseases, including rheumatological, neurological, neuromuscular, cardiovascular, haematological, nephrological and metabolic. Production of a variety of autoantibodies has been demonstrated to occur during B19 infection and these have been shown to be key to the pathogenesis of the particular disease process in a significant number of cases, for example, production of rheumatoid factor in cases of B19-associated rheumatoid arthritis and production of anti-glutamic acid decarboxylase (GAD) in patients with B19-associated type 1 diabetes mellitus. B19 infection has also been associated with the development of multiple autoimmune diseases in 12 individuals. Documented mechanisms in B19-associated autoimmunity include molecular mimicry (IgG antibody to B19 proteins has been shown to cross react with a variety of recognised human autoantigens, including collagen II, keratin, angiotensin II type 1 receptor, myelin basic protein, cardiolipin, and platelet membrane glycoprotein IIb/IIIa), B19-induced apoptosis with presentation of self-antigens to T lymphocytes, and the phospholipase activity of the B19 unique VP1 protein.