Jason L. Wang

BioE Ph.D. Defense Presentation

Thursday, April 26th, 2018, 2:00pm

IBB Building, Room 1128

Advisor: 

Robert E. Guldberg, Ph.D. (Mechanical Engineering, Georgia Institute of Technology)

Committee:

Rudolph L. Gleason, Ph.D. (Mechanical Engineering, Georgia Institute of Technology)

Manu O. Platt, Ph.D. (Biomedical Engineering, Georgia Institute of Technology)

Johnna S. Temenoff, Ph.D. (Biomedical Engineering, Georgia Institute of Technology)

M. Neale Weitzmann, Ph.D. (School of Medicine, Emory University)

Skeletal Development and Bone Healing in HIV-1 Transgenic Rodent Models

HIV and AIDS have drastically compromised the quality of life and lifespan for millions of people worldwide. Effective antiretroviral therapy has dramatically increased the life expectancy of those infected with HIV to nearly that of the general population. A positive HIV diagnosis with appropriate treatment is now a chronic condition bringing with it the premature onset of disorders traditionally associated with the natural aging process including osteoporosis. It is well understood that HIV infection is a risk factor for osteopenia and osteoporosis, and more recent studies have established an increase in fracture prevalence in the HIV-infected population. However, the effects of HIV infection on bone are difficult to investigate in the clinical setting. Traditional risk factors for osteoporosis can complicate any observed effects that HIV may have. Despite the increased risk for fracture and fracture prevalence in the HIV-infected population, a paucity of studies has investigated the potential for HIV infection to adversely affect fracture healing.

The main goal of this work was to investigate the effects of HIV on skeletal growth and bone healing as exhibited by the HIV-1 transgenic mouse and rat models. In addition to the extensive body of bone research conducted in mouse and rat models, the transgenic rodent models offer significant advantages for pre-clinical research over the more recognized infectious non-human primate and humanized mouse models including less time and expense. Thus, we first characterized the skeletal phenotype in the HIV-1 transgenic mouse model by evaluating bone microarchitecture and biomechanics. We further assessed whether HIV mice present with impairment in long bone fracture healing. Second, we characterized the longitudinal skeletal changes in the growing HIV-1 transgenic rat. Finally, we investigated alterations to bone healing in the HIV-1 transgenic rat using a critically-sized segmental bone defect model. Taken together, this thesis has provided evidence for the use of the HIV-1 transgenic rodent models for pre-clinical investigations into skeletal disorders in the context of HIV.

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