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Clinical Microbiology Reviews, July 2002, p. 485-505, Vol. 15, No. 3
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.3.485-505.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Human Parvovirus B19

Erik D. Heegaard1 and Kevin E. Brown2**

Department of Clinical Microbiology, University State Hospital, Rigshospitalet, Copenhagen, Denmark,,1 Hematology Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland2

Parvovirus B19 (B19) was discovered in 1974 and is the only member of the family Parvoviridae known to be pathogenic in humans. Despite the inability to propagate the virus in cell cultures, much has been learned about the pathophysiology of this virus, including the identification of the cellular receptor (P antigen), and the control of the virus by the immune system. B19 is widespread, and manifestations of infection vary with the immunologic and hematologic status of the host. In healthy immunocompetent individuals B19 is the cause of erythema infectiosum and, particularly in adults, acute symmetric polyarthropathy. Due to the tropism of B19 to erythroid progenitor cells, infection in individuals with an underlying hemolytic disorder causes transient aplastic crisis. In the immunocompromised host persistent B19 infection is manifested as pure red cell aplasia and chronic anemia. Likewise, the immature immune response of the fetus may render it susceptible to infection, leading to fetal death in utero, hydrops fetalis, or development of congenital anemia. B19 has also been suggested as the causative agent in a variety of clinical syndromes, but given the common nature, causality is often difficult to infer. Diagnosis is primarily based on detection of specific antibodies by enzyme-linked immunosorbent assay or detection of viral DNA by dot blot hybridization or PCR. Treatment of persistent infection with immunoglobulin reduces the viral load and results in a marked resolution of anemia. Vaccine phase I trials show promising results.

* Corrresponding author. Mailing address: Hematology Branch, NHLBI, Bldg. 10/Room 7C218, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892-1652. Phone: (301) 496-2479. Fax: (301) 496-8396. E-mail: brownk{at}nhlbi.nih.gov.

Clinical Microbiology Reviews, July 2002, p. 485-505, Vol. 15, No. 3
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.3.485-505.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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Copyright © 2002 by the American Society for Microbiology. All rights reserved.