B19 virus shows a tropism for two types of cells: (a) red blood cell (RBC) precursors and (b) endothelial cells in the blood vessels.
The virus infects rapidly dividing erythrocyte precursors, such as bone marrow cells, erythroid cells from fetal liver, and ery-throid leukemia cells, and destroys these cells after infection, thereby causing aplastic anemia. Infection of the endothelial cells in the blood vessels leads to erythema infectiosum. It has been demonstrated that the B19 virus first enters through the nasopharynx or upper respiratory tract and then spreads to the blood, causing viremia. The virus then infects mitotically active erythroid precursor cells in bone marrow and establishes the infection.
The virus enters susceptible cells through the P blood antigen receptors on the erythrocyte precursors. Inside the red cells, the virus enters the nucleus, starts replicating, followed by killing of the red cells. The production of RBCs is stopped for approximately 1 week due to killing of the erythroid precursor cells by the viruses. The initial stage is associated with flu-like illness caused by large viremia. The viruses are shed in the oral and respiratory secretions and even cross the placenta. Subsequently, viremia is controlled by the production of specific antibodies against B19 virus.
The rash and arthralgia present the second stage of the disease and is believed to be immunologically mediated. This stage coincides with the disappearance of B19 virus from the circulation, appearance of B19 virus-specific IgM and IgG antibodies, and finally the formation of immune complexes.
The disease exhibits two stages: initial stage is flu-like illness and second stage is appearance of rash and arthralgia. Host immunity to B19 virus infection is primarily antibody medi-ated. The circulating antibodies stop the viremia and are impor-tant for resolution of the disease. The role of cell-mediated immunity in conferring immunity to B19 virus is unknown.
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