College of Natural Sciences

Department of Microbiology

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Welcome to the Hoang Lab Website!

Snyder Hall

The University of Hawaii at Manoa is located in the beautiful Manoa Valley and five minutes away from world famous Waikiki Beach. Our laboratories are located at the Manoa campus and the new John A. Burns School of Medicine.


We are always interested in motivated, intelligent, and innovative prospective graduate students and postdoctoral fellows.


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Education

B.Sc. Biochemistry, University of Calgary, 1994


M.Sc. Microbiology and Infectious Diseases, University of Calgary, 1996


Ph.D. Microbiology, Colorado State University, 2000


Specialization

Microbiology and Bacterial Genetics and Molecular Pathogenesis



Research Interests

The Hoang Lab currently has two areas of infectious disease research interests, focusing on the genetics and pathophysiology of i) Burkholderia pseudomallei and ii) Pseudomonas aeruginosa:


i) B. pseudomallei is a CDC category B and potential bioterrorism agent, causing a disease called melioidosis throughout the tropical regions mainly in Southeast Asia and Northern Australia. The disease resembles and can be misdiagnosed for tuberculosis. This bacterium can often be isolated from the water and soil of rice fields (panel A) and other environments throughout the tropical regions. The organism can be aerosolized and mortality rates of infected patients can be as high as 50-90%; thus, precautions to prevent inhalation in the laboratory are necessary (panel B and C).


The lab currently researches the molecular pathogenesis of B. pseudomallei during its infection within host-cells. Our hypothesis is that B. pseudomallei, as it encounters and senses uniquely different intracellular environments and performs sequential steps in the infection process, will undergo differential gene expression at each stage of intracellular cycle. We pioneered and studied global transcriptional profiling of single B. pseudomallei cells as it transit through the host cell, which we cumulatively named a “transitome.” Our goal is to more clearly identify the genes, and hence the proteins, required for eukaryotic hosts’ cellular infection in each spatially defined infectious stage (vesicle, cytoplasm, and membrane protrusion; panels E-H). Ultimately, understanding the function of these virulence genes and mechanisms of infection and disease at the molecular level will aid in rational drug and vaccine design.


The lab also has pioneered, successfully tested, and published several molecular genetic tools, aiding molecular genetic studies in B. pseudomallei and other Burkholderia species. The ease of genetic manipulations of B. pseudomallei using these tools will expand research that will contribute to molecular genetics, pathogenesis, and bacteria-host interaction studies crucial for the discovery of novel vaccines, therapeutics, and diagnostic targets.


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B

Student in lab.

C



ii) P. aeruginosa is an opportunistic pathogen of plants, animals, and humans. The major focus of this second research topic in the lab involves P. aeruginosa in Cystic Fibrosis (CF) lung infection. P. aeruginosa has the ability to obtain nutrients in the CF lung for high-cell-density (HCD) replication (>109 cfu/mL of sputum), leading to quorum-sensing controlled virulence expression. The long-term goal is to define the metabolic capability of P. aeruginosa within the CF lung and the host pulmonary nutrient factors that contribute to HCD replication. Our hypothesis is that P. aeruginosa utilizes surfactant lipids as one of the available nutrient and energy sources, affording replication and maintenance at HCD. The rationale is that knowledge of the pathophysiology of P. aeruginosa, contributing to lung surfactant lipid degradation for HCD replication, would lead to innovative approaches for improved treatment extending the lives of CF patients who suffer from debilitating and fatal chronic lung infections.

Charts

Lung surfactant components (90% lipids and 10% proteins), especially lipids, are absolutely essential for normal pulmonary function. Of the 90% lipids in lung surfactant, 80% is phosphatidylcholine (PC). The lipid component of lung surfactant (i.e., PC) is readily metabolized by P. aeruginosa in vitro. Phospholipases and lipases, required for PC degradation, are essential virulence determinants expressed in vivo to degrade PC into three constituents (fatty acid, glycerol, and phosphorylcholine). All three constituents are also readily metabolized by P. aeruginosa in vitro. The metabolism of glycerol and phosphorylcholine is fairly well characterized. However, the pathways through which fatty acid (FA) constituents of PC are further metabolized by P. aeruginosa are undefined. The research in the lab currently focuses on establishing the importance of FA degradation pathways of P. aeruginosa and their contributions to bacterial in vivo replication.