Gerry Andrews, Ph.D.
Assistant Professor
Veterinary Sciences, Medical Microbiologist

B.S., Pennsylvania State University
M.S., University of New Hampshire
Ph.D., Uniformed Services University of the Health Sciences
gandrews@uwyo.edu • [CV] • (307) 766-3139 • AG C #6004

Research Interests:

Role of bacterial secretion systems in pathogenesis

I am currently studying the chaperone-usher "secreton" of Yersinia pestis which facilitates synthesis and formation of the protein capsule (F1 antigen) on the surface of the microorganism. Preliminary data suggest a role for the operon's accessory genes beyond secretion and morphogenesis of the F1 capsule. Experiments are planned to further address this hypothesis. My future interests also include examining other secretion systems in the yersiniae, as well as characterization of the mechanisms of protein secretion in F. tularensis and B. abortus.

Identification and characterization of new/novel virulence determinants of bacterial pathogens (with emphasis on select agents)

Specifically, I am interested in characterization of selected genes and their products from the high molecular weight virulence plasmid (pFra) of Y. pestis, and the assessment of their role in the pathogenesis of plague. Additionally, I am interested in the identification and characterization of in vivo expressed antigens using In Vivo Induced Antigen Technology (IVIAT). These studies are planned for Y. pestis, F. tularensis, and B. abortus.

Determining the basis of protective immunity in the host against plague antigens

I am continuing with studies to assess protective host immunity against plague by a variety of Y. pestis antigens, to include to plasmid-encoded virulence proteins, YopD and YpkA. I am completing a collaborative project on the analysis of the human antibody response (antigenic profiling) to bubonic and pneumonic plague by ELISA and immunoblot with human convalescent sera.

Pathoadaptive evolution of bacterial select agents

This area of research involves the identification/characterization of genetic loci, when inactivated will increase fitness of the pathogen in the host. I intend to examine this phenomenon in Y. pestis, F. tularensis, and Brucella spp.

Teaching:

MICR 2220 • Pathogenic Microbiology