Wagstaff, Reece2011-05-162011-05-162011-04-13https://hdl.handle.net/11299/104509Additional contributors: Arun Sasikala; Hyeon Kim; JJ Hong; Ashley Haase; R. Paul Johnson; Jung Jo Hong; Pamela J. Skinner (faculty mentor)Human immunodeficiency virus (HIV) was identified as the cause of acquired immunodeficiency syndrome (AIDS) in the 1980s, and since then it has proliferated into one of the most vexing pandemics of its time, if not all of human history. As of today, there is still no known cure for HIV, although numerous strategies are currently being pursued to confer immunity. Vaccines represent one of those strategies, and are a plausible method for bestowing resistance to HIV and other lentiviruses. Currently, research exists to show that attenuated vaccines created from simian immunodeficiency virus (SIV), an HIV analogue present in simians such as the Rhesus Macaque, provide suitable resistance for that disease in the simian model. Being that the SIV genome is sufficiently similar to the HIV genome, there is a good probability that an attenuated vaccine created from HIV could produce comparable immunity in humans, however, the mechanism by which SIV vaccines confer resistance is still not well understood and needs to be studied further if attenuated HIV vaccines are ever to be presented in human clinical trials. My hypothesis is that an early, robust, SIV-specific CD8 T cell response in lymph nodes and in the site of infection is responsible for the protection induced from live-attenuated SIV vaccines. To test this hypothesis I quantified perforin assays in lymphatic tissues of immunized macaques that have been challenged with pathogenic SIV. The assays were created by immunohistochemistry staining techniques, including in-situ tetramer staining, and evaluated via scanning confocal microscopy.en-USCollege of Liberal ArtsDepartment of EnglishCollege of Veterinary MedicineDepartment of Veterinary and Biomedical SciencesPresentation