What is the pathophysiology of parvovirus B19 (B19V) infection?

Updated: Oct 11, 2019
  • Author: David J Cennimo, MD, FAAP, FACP, AAHIVS; Chief Editor: Russell W Steele, MD  more...
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Parvovirus B19 has a unique tropism for human erythroid progenitor cells. The virus requires the P blood antigen receptor (also known as globoside) to enter the cell. Rare individuals who lack the P antigen are immune to parvovirus B19 infection. Once inside the host cell, viral DNA enters the nucleus. The 3' end of the DNA strand folds back on itself, forming a hairpinlike bend that functions as a self-primer for viral DNA replication. The virus is cytotoxic to host cells. [2, 12] This, coupled with the tropism for rapidly dividing erythrocyte precursors (particularly pronormoblasts and normoblasts, wherein they replicate to high titers), leads to the suppression of erythrogenesis seen during infection. No reticulocytes (immature erythrocytes) are available to replace aging or damaged erythrocytes as they are cleared by the reticuloendothelial system. [5, 2]

Although decreases in hemoglobin levels of greater than 1 g/dL are rare in healthy children infected with parvovirus B19, decreases of 2-6 g/dL may be observed in patients with hemoglobinopathies or hemolytic anemias. Occasionally, the virus infects leukocytes (especially neutrophils). [13] Parvovirus B19 does not infect megakaryocytes; however, in vitro, parvovirus B19 proteins have a cytotoxic effect on megakaryocytes. Although B19V infection may manifest with pancytopenia, it is not believed to contribute significantly as an etiology of true aplastic anemia. [9, 11]

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