[Human parvovirus B19 as the cause of aplastic crisis in hereditary spherocytosis]. / Humant parvovirus B19 som årsak til aplastisk krise ved hereditaer sfaerocytose.

A seven months old boy was admitted to hospital for investigation and treatment of severe anaemia. The final diagnosis was hereditary spherocytosis. When, six weeks later, he developed an aplastic crisis, serological criteria provided evidence of recent human parvovirus B19 infection. The same disease was detected in the family. Human parvovirus B19 is shown to be of particular interest in aplastic crisis.

Inhibition of erythropoiesis by human parvovirus-containing serum from a patient with hereditary spherocytosis in aplastic crisis.

Aplastic phase serum from a patient with aplastic crisis of hereditary spherocytosis, which was demonstrated to contain human parvovirus, inhibited in vitro erythroid colony formation almost completely. Human parvovirus was resistant to heating for 30 min at 56 degrees C. The suppressive effect of the serum was completely abrogated by adding convalescent phase serum from another patient with aplastic crisis of hereditary spherocytosis. Some normal sera had similar neutralizing ability. The results suggested that aplastic crisis of a patient with hereditary spherocytosis is caused by human parvovirus and that the neutralizing test could offer a tool for predicting the future occurrence of aplastic crisis in the patients with chronic hemolytic anemia.

A human parvovirus-like virus inhibits haematopoietic colony formation in vitro.

Viruses have been shown to cause bone marrow aplasia in animals and have been implicated in bone marrow failure in man; however, until recently, a specific link between human viral infection and bone marrow failure has not been proven. In 1975 Cossart and colleagues found a serum parvovirus-like virus (SPLV, sometimes referred to as B19) in human serum. Antibody to this virus is present in the sera of 30-45% of healthy adults (Y. E. Cossart, P. P. Mortimer, unpublished observations). However, evidence for a direct link came from work by Pattison et al. who found five children with transient aplastic crisis of sickle cell disease and evidence of active infection with SPLV. This association was later confirmed in a large series of children with sickle cell disease and aplastic crisis in Jamaica. We have studied the effects of virus-containing material on haematopoiesis, using in vitro colony-forming assays to look for direct evidence for a role of SPLV in bone marrow aplasia. We show here that SPLV-containing sera inhibit erythropoiesis in culture. Moreover, in a child with hereditary spherocytosis who developed transient aplastic crisis, a strong inhibitory effect of the patient's serum on erythropoiesis correlated with the presence of virus.