Our laboratory performs basic and clinical studies of the B19 parvovirus, the only member of parvoviradae family pathogenic in humans. Acute infection causes fifth disease, a childhood rash illness and a polyarthralgia syndrome in adults. In patients with underlying hemolysis, acute infection results in transient aplastic crisis. In patients with underlying immunodeficiency, virus infection persists and causes chronic anemia; parvovirus infection is a cause of anemia in patients with AIDS. The virus is trophic for erythroid progenitor cells. We have made progress in B19 parvovirus biology in a number of areas over the last year. We have discovered the first case of congenital B19 parvovirus infection: transmission of the virus to the fetus resulted in chronic anemia at birth and death at 7 months; virus was restricted to the marrow and did not circulate. The recovery of an adult patient with congenital pure red cell aplasia, whose bone marrow showed B19 parvovirus, suggests that interleukin-3 may induce antibody formation to this virus, possibly of use in patients with AIDS-associated infection. We have induced neutralizing antibodies to B19 parvovirus using baculovirus-generated empty capsids in animals. This empty capsid system can be manipulated to increase the proportion of the minor capsid protein the minor capsid protein antigen contains a neutralizing epitope Because it is not required for virus assembly, substitution of heterologous proteins sequences in the unique region of the minor capsid antigen make empty parvovirus capsids useful as vaccine agents and for specific delivery of proteins. we have achieved propagation of B19 parvovirus outside of bone marrow using a megakaryocyte cell line derived from a patient with leukemia. The trophism of parvovirus for erythroid cells has been investigated at the molecular level. Based on the pattern of RNA transcription in cells transfected with parvovirus sequences, the function of the p(6) promotor in nonpermissive cells, and deletion mutations analyzed by RNA protection, we have concluded that a block in transcription in the middle of the genome exists in nonpermissive cells, possibly at an attenuator region downstream from the nonfunctional P44 promoter.
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