This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Heegaard, E. D.
Right arrow Articles by Brown, K. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Heegaard, E. D.
Right arrow Articles by Brown, K. E.

 Previous Article  |  Next Article 

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.



This article has been cited by other articles:

  • Mingozzi, F., Meulenberg, J. J., Hui, D. J., Basner-Tschakarjan, E., Hasbrouck, N. C., Edmonson, S. A., Hutnick, N. A., Betts, M. R., Kastelein, J. J., Stroes, E. S., High, K. A. (2009). AAV-1-mediated gene transfer to skeletal muscle in humans results in dose-dependent activation of capsid-specific T cells. Blood 114: 2077-2086 [Abstract] [Full Text]  
  • Duechting, A., Tschope, C., Kaiser, H., Lamkemeyer, T., Tanaka, N., Aberle, S., Lang, F., Torresi, J., Kandolf, R., Bock, C.-T. (2008). Human Parvovirus B19 NS1 Protein Modulates Inflammatory Signaling by Activation of STAT3/PIAS3 in Human Endothelial Cells. J. Virol. 82: 7942-7952 [Abstract] [Full Text]  
  • Norja, P., Eis-Hubinger, A. M., Soderlund-Venermo, M., Hedman, K., Simmonds, P. (2008). Rapid Sequence Change and Geographical Spread of Human Parvovirus B19: Comparison of B19 Virus Evolution in Acute and Persistent Infections. J. Virol. 82: 6427-6433 [Abstract] [Full Text]  
  • Schneider, B., Hone, A., Tolba, R. H., Fischer, H.-P., Blumel, J., Eis-Hubinger, A. M. (2008). Simultaneous persistence of multiple genome variants of human parvovirus B19. J. Gen. Virol. 89: 164-176 [Abstract] [Full Text]  
  • Bruggeman, L. A. (2007). Viral Subversion Mechanisms in Chronic Kidney Disease Pathogenesis. CJASN 2: S13-S19 [Abstract] [Full Text]  
  • Parsyan, A., Szmaragd, C., Allain, J.-P., Candotti, D. (2007). Identification and genetic diversity of two human parvovirus B19 genotype 3 subtypes. J. Gen. Virol. 88: 428-431 [Abstract] [Full Text]  
  • Bastien, N., Chui, N., Robinson, J. L., Lee, B. E., Dust, K., Hart, L., Li, Y. (2007). Detection of Human Bocavirus in Canadian Children in a 1-Year Study. J. Clin. Microbiol. 45: 610-613 [Abstract] [Full Text]  
  • Lupescu, A., Bock, C.-T., Lang, P. A., Aberle, S., Kaiser, H., Kandolf, R., Lang, F. (2006). Phospholipase A2 Activity-Dependent Stimulation of Ca2+ Entry by Human Parvovirus B19 Capsid Protein VP1. J. Virol. 80: 11370-11380 [Abstract] [Full Text]  
  • Toan, N. L., Duechting, A., Kremsner, P. G., Song, L. H., Ebinger, M., Aberle, S., Binh, V. Q., Duy, D. N., Torresi, J., Kandolf, R., Bock, C.-T. (2006). Phylogenetic analysis of human parvovirus B19, indicating two subgroups of genotype 1 in Vietnamese patients.. J. Gen. Virol. 87: 2941-2949 [Abstract] [Full Text]  
  • Espy, M. J., Uhl, J. R., Sloan, L. M., Buckwalter, S. P., Jones, M. F., Vetter, E. A., Yao, J. D. C., Wengenack, N. L., Rosenblatt, J. E., Cockerill, F. R. III, Smith, T. F. (2006). Real-Time PCR in Clinical Microbiology: Applications for Routine Laboratory Testing. Clin. Microbiol. Rev. 19: 165-256 [Abstract] [Full Text]  
  • Norbeck, O., Isa, A., Pohlmann, C., Broliden, K., Kasprowicz, V., Bowness, P., Klenerman, P., Tolfvenstam, T. (2005). Sustained CD8+ T-Cell Responses Induced after Acute Parvovirus B19 Infection in Humans. J. Virol. 79: 12117-12121 [Abstract] [Full Text]  
  • Candotti, D., Etiz, N., Parsyan, A., Allain, J.-P. (2004). Identification and Characterization of Persistent Human Erythrovirus Infection in Blood Donor Samples. J. Virol. 78: 12169-12178 [Abstract] [Full Text]  
  • Young, N. S., Brown, K. E. (2004). Parvovirus B19. NEJM 350: 586-597 [Full Text]  
  • Schorling, S., Schalasta, G., Enders, G., Zauke, M. (2004). Quantification of Parvovirus B19 DNA Using COBAS AmpliPrep Automated Sample Preparation and LightCycler Real-Time PCR. J. Mol. Diagn. 6: 37-41 [Abstract] [Full Text]  
  • Weigel-Kelley, K. A., Yoder, M. C., Srivastava, A. (2003). {alpha}5{beta}1 integrin as a cellular coreceptor for human parvovirus B19: requirement of functional activation of {beta}1 integrin for viral entry. Blood 102: 3927-3933 [Abstract] [Full Text]  
  • Segovia, J. C., Guenechea, G., Gallego, J. M., Almendral, J. M., Bueren, J. A. (2003). Parvovirus Infection Suppresses Long-Term Repopulating Hematopoietic Stem Cells. J. Virol. 77: 8495-8503 [Abstract] [Full Text]  
  • Lopez-Bueno, A., Mateu, M. G., Almendral, J. M. (2003). High Mutant Frequency in Populations of a DNA Virus Allows Evasion from Antibody Therapy in an Immunodeficient Host. J. Virol. 77: 2701-2708 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»