Regular Article
Haematological consequences of parvovirus B19 infection

https://doi.org/10.1053/beha.1999.0071Get rights and content

Abstract

Parvovirus B19, a member of the Erythrovirus genus, is the only member of theParvoviridae family known to be pathogenic in humans. Erythroviruses are so named because of their tropism and selective replication in erythroid progenitor cells. Haematological consequences of B19 infection arise due to a direct cytotoxic effect on erythroid progenitors in bone marrow with interruption of erythrocyte production. In addition, the physiology of host haematopoiesis and competence of the immune response each determines clinical manifestations of B19 infection: in individuals with underlying haemolytic disorders, B19 infection causes transient aplastic crisis; in immunocompromised patients, persistent B19 infection may develop that manifests as pure red cell aplasia and chronic anaemia; B19 infection in utero may result in fetal death, hydrops fetalis, or congenital anaemia. Diagnosis is based on examination of bone marrow and B19 virological studies. Treatment of persistent infection with immunoglobulin leads to a prompt resolution of the anaemia.

References (80)

  • GA Luzzi et al.

    Human parvovirus arthropathy and rheumatoid factor

    Lancet

    (1985)
  • M Soderlund et al.

    Persistence of parvovirus B19 DNA in synovial membranes of young patients with and without chronic arthropathy

    Lancet

    (1997)
  • DS Pardi et al.

    Hepatitis-associated aplastic anemia and acute parvovirus B19 infection: a report of two cases and a review of the literature

    American Journal of Gastroenterology

    (1998)
  • EM Sokal et al.

    Acute parvovirus B19 infection associated with fulminant hepatitis of favourable prognosis in young children

    Lancet

    (1998)
  • SJ Naides et al.

    Human parvovirus B19 infection and hepatitis

    Lancet

    (1996)
  • J Bernuau et al.

    Parvovirus B19 infection and fulminant hepatitis

    Lancet

    (1999)
  • Y Yoto et al.

    Human parvovirus B19 infection associated with acute hepatitis

    Lancet

    (1996)
  • AN Langnas et al.

    Parvovirus B19 as a possible causative agent of fulminant liver failure and associated aplastic anemia

    Hepatology

    (1995)
  • GJ Kurtzman et al.

    Persistent B19 parvovirus infection as a cause of severe chronic anaemia in children with acute lymphocytic leukaemia

    Lancet

    (1988)
  • JA Jordan

    Identification of human parvovirus B19 infection in idiopathic nonimmune hydrops fetalis

    American Journal of Obstetrics and Gynecology

    (1996)
  • KE Brown et al.

    Congenital anaemia after transplacental B19 parvovirus infection

    Lancet

    (1994)
  • MJ Anderson et al.

    An outbreak of erythema infectiosum associated with human parvovirus infection

    Journal of Hygiene

    (1984)
  • N Okabe et al.

    Detection of antibodies to human parvovirus in erythema infectiosum (fifth disease)

    Archives of Disease in Childhood

    (1984)
  • FA Plummer et al.

    An erythema infectiosum-like illness caused by human parvovirus infection

    New England Journal of Medicine

    (1985)
  • G Siegl et al.

    Characteristics and taxonomy of Parvoviridae

    Intervirology

    (1985)
  • KI Berns et al.

    Family Parvoviridae

  • MG O'Sullivan et al.

    Identification of a novel simian parvovirus in cynomolgus monkeys with severe anemia: a paradigm of human B19 parvovirus infection

    Journal of Clinical Investigation

    (1994)
  • MG O'Sullivan et al.

    Experimental infection of cynomolgus monkeys with simian parvovirus

    Journal of Virology

    (1997)
  • KE Brown et al.

    The simian parvoviruses

    Reviews in Medical Virology

    (1997)
  • K Ozawa et al.

    Novel transcription map for the B19 (human) pathogenic parvovirus

    Journal of Virology

    (1987)
  • K Ozawa et al.

    Replication of the B19 parvovirus in human bone marrow cell cultures

    Science

    (1986)
  • K Ozawa et al.

    Characterization of capsid and noncapsid proteins of B19 parvovirus propagated in human erythroid bone marrow cell cultures

    Journal of Virology

    (1987)
  • S Moffatt et al.

    Human parvovirus B19 nonstructural (NS1) protein induces apoptosis in erythroid lineage cells

    Journal of Virology

    (1998)
  • N Sol et al.

    Possible interactions between the NS-1 protein and tumour necrosis factor alpha pathways in erythroid cell apoptosis induced by human parvovirus B19

    Journal of Virology

    (1999)
  • S Kajigaya et al.

    Self-assembled B19 parvovirus capsids, produced in a baculovirus system, are antigenically and immunogenically similar to native virions

    Proceedings of the National Academy of Sciences of the USA

    (1991)
  • PR Chipman et al.

    Cryo-electron microscopy studies of empty capsids of human parvovirus B19 complexed with its cellular receptor

    Proceedings of the National Academy of Sciences of the USA

    (1996)
  • SJ Rosenfeld et al.

    Unique region of the minor capsid protein of human parvovirus B19 is exposed on the virion surface

    Journal of Clinical Investigation

    (1992)
  • K Umene et al.

    Genetic diversity of human parvovirus B19 determined using a set of restriction endonucleases recognizing four or five base pairs and partial nucleotide sequencing: use of sequence variability in virus classification

    Journal of General Virology

    (1991)
  • DD Erdman et al.

    Genetic diversity of human parvovirus B19: sequence analysis of the VP1/VP2 gene from multiple isolates

    Journal of General Virology

    (1996)
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