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Efficacy Of The New Yersinia Pestis Subunit Vaccine In Animal Models Of Plague | 5394
ISSN: 2157-2526

Journal of Bioterrorism & Biodefense
Open Access

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Efficacy of the new Yersinia pestis subunit vaccine in animal models of plague

International Conference on Biothreats & Biodefense

Kei Amemiya

Keynote: J Bioterr Biodef

DOI: 10.4172/2157-2526.S1.001

Abstract
Until recently, the vaccine against Yersinia pestis, the etiological agent of plague, consisted of a formalin-inactivated, whole-cell vaccine. The vaccine was discontinued because it apparently only protected the vaccinated host against bubonic plague but not pneumonic plague. We have since found that the whole-cell vaccine only induced antibodies against the capsule F1 protein but not antibodies against the virulence protein (V-antigen) that appears to be required for a robust protection. The new plague vaccine consists of subunits of the F1 capsule protein and V-antigen either as individual subunits or a fusion of the two subunits. The genes for each these proteins are encoded on two separate virulence plasmids; one of the plasmids is specific for Y. pestis. Initially, it was proposed that only antibodies against the vaccine subunits were sufficient for protection against an exposure to the pathogen. Part of this reasoning was from studies with immune serum or monoclonal antibodies against the F1 or V-antigen subunits that showed that these sources of antibodies can passively protect an animal against a plague infection. Nevertheless, we have shown that the participation of the innate immune system is required for complete protection against a pneumonic plague challenge with Y. pestis CO92 a fully virulent strain of plague. Although it is not completely clear how protection is mediated by the new subunit vaccine, the subunit vaccine has been through a Phase IIa human clinical trial. We will present the efficacy of the new Y. pestis plague subunit vaccine in two animal models of plague
Biography
Amemiya received his doctoral degree from Rutgers University in Microbiology in 1973. He did his post-graduate studies in gene regulation in the laboratory of Lucy Shapiro at Albert Einstein College of Medicine, Bronx, N.Y. Later, he went to the National Institute of Neurological Diseases and Stroke in 1986, where he examined gene regulation in JC virus that caused the demyelinating disease progressive multifocal leukoencephalopathy in immune suppressed patients. In 1999, he went to the U.S. Army Medical Research Institute of Infectious Diseases, Bacteriology Division, where he has been involved in vaccine development for Burkholderia mallei and Yersinia pestis. His primary interest has been in the immune response and innate immunity in animal models.
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