Our laboratory performs basic and clinical studies of the B19 parvovirus, the only member of the 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 tropic for erythroid progenitor cells. We have made progress in B19 parvovirus biology in a number of areas over the last year. First, using a unique human cell line called UT-7, in which we had previously shown propagation of B19 parvovirus, we have demonstrated that the virus can remain latent in cells. Furthermore, when these cells are infected, B19 parvovirus genes are expressed sequentially with early and late RNA production. Abortive infection probably represents selective expression of early gene. Second, in vaccine studies we have shown that recombinant parvovirus capsids can elicit neutralizing antibodies in three animal species. Furthermore, the VP1 unique region, which is external to the capsid, is required for neutralizing antibody formation. Several lines of evidence indicate that VP1 not only introduces its own neutralizing epitope sequences into the capsid but alters the recognition of VP2 sequences by allosteric effects. A hypothesis has been formulated that VP1 is required for cell surface receptor binding or for unncoating of virus genetic material. Third, we have succeeded in substituting large regions of heterologous protein for the unique region of VP1 in an effort to develop empty parvovirus capsids as platforms for protein presentation. Finally, some progress has been made towards identification of the virus receptor for B19 parvovirus.
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