Journal of Vaccines & Vaccination

Development of a mutated human parvovirus B19 vaccine to prevent aplastic anemia in congenital and acquired anemias

10^th Euro Global Summit and Expo on Vaccines & Vaccination

June 16-18, 2016 Rome, Italy

Alfred Bennett Jenson and Shin-je Ghim

University of Louisville, USA

Posters & Accepted Abstracts: J Vaccines Vaccin

Abstract:

Human parvovirus B19, the only human erythrovirus, targets a blood group globoside on progenitor red blood cells causing congenital abnormalities and aplastic anemia in a pleothra of individuals with congenital and acquired anemias. B19 recombinant capsid vaccines, that were composed of wild type VP1 and 2, have been associated with adverse side effects and low immunogenicities. Unlike other parvoviruses (eg., canine, porcine), B19 has a unique viral ligand, P-antigen binding site, that is located in the recess of the 3-fold axis of the virion. B19V virions and virus like particles (VLPs) bind to a blood group globoside, P-antigen, predominantly expressed on immature and mature red blood cells of humans. We hypothesize that binding of the B19 capsid to the blood group globoside causes a structural change in the neutralizing conformationally dependent epitopes permitting infection of erythroid precursors and development of aplastic anemia. To prevent attachment of B19 to globosides and facilitate development of an efficacious vaccine, we mutated the ligand, P-antigen binding site, on VP2 major capsid protein that is responsible for binding to precursor and mature RBCs and generated VLPs, that are incapable of inducing hemagglutination, using baculovirus expression system. We now present the structural analysis of the mutated B19 capsid, and preliminary data on its antigenicity.

Biography :

Email: ab.jenson@affinicorp.com