Parvovirus B19 diseases arise either from direct viral toxicity for specific target cells or as a result of the host immune response (Table 1). Direct viral infection leads to destruction of marrow erythroid cells in normal individuals, but cessation of red cell production is short-lived due to rapid immune clearance of virus, and the long lifespan of erythrocytes precludes the development of anemia.
In many persons, B19 infection is asymptomatic. Fifth disease in children presents typically with a 'slapped cheek' appearance and a lacy, evanescent maculopapular cutaneous eruption. Adults more often present with a polyarthralgia/polyarthritis syndrome. Rash and arthropathy are usually transient but may recur for several weeks or months; some women have had a relapsing chronic rheumatic syndrome that resembled rheumatoid arthritis. Normal volunteer studies showed that both the rash and arthropathy develop concomitantly with the rise in antiviral antibodies, and in patients with community-acquired fifth disease who have circulating specific IgM antibody, parvovirus is difficult to recover. These results suggest that fifth disease is immune complex-mediated.
In contrast, direct viral toxicity dominates the clinical picture in individuals with a shortened red cell life span, usually as a consequence of inherited hemolytic anemia such as sickle cell disease or hereditary spherocytosis. In these patients, cessation of red cell production causes an abrupt, occasionally fatal worsening of chronic anemia called transient aplastic crisis (TAC). The self-limited character of the illness is due to the development of neutralizing antibodies which terminate the infection. TAC is rarely followed by fifth disease symptoms, perhaps because the large amount of virus produced by the expanded erythroid bone marrow is unfavorable for antibody-antigen lattice formation and immune complex deposition. Variations in the antibody response may also account for the lack of symptoms in about 25% of normal persons with acute parvovirus infection.
Both the normal volunteer and epidemiologic investigations demonstrated that the same virus was responsible for different clinical syndromes. Virus variability is probably not important pathophysio-logically, since multiple isolates have been shown to be very similar at the nucleotide level and as antigens, and minor differences on restriction enzyme mapping have not been correlated with different clinical syndromes.
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