Thesis advisor: Kenneth Williams / Approximately 15% of individuals infected with Human Immunodeficiency Virus (HIV) develop a neurological condition that consists of motor dysfunction and cognitive deterioration in late stage disease that is known as the AIDS dementia complex (ADC). This condition is mirrored in rhesus macaques infected with Simian Immunodeficiency Virus (SIV), which can be more easily studied. This project analyzed different macrophage populations in rhesus macaques infected and uninfected with SIV at early and terminal stage disease. Single and double immunohistochemistry stains were performed for the known macrophage and microglial markers CD163, CD16, CD68, Mac387, HAM56, and Iba-1, as well as for the SIV-p28 viral protein. Photographs and observations of the tissue stainings demonstrated that early after infection with SIV, there is an increase in perivascular macrophages and monocytes surrounding vessels and tissue edges, and the SIV-p28 protein is already present. There is also an observed change in the morphology of the microglia to an active, ramified state. After the development of AIDS and SIVE, the increase in all of the macrophage markers and the accumulation of activated microglia are clearly visible, especially surrounding and within lesions. Furthermore, these markers can be used to categorize the encephalitic lesions as “new” or “old” based on the presence or absence of Mac387 within the cells. All lesions contained CD68+ and HAM56+ macrophages, but “new” lesions presented with a relatively high count of Mac387+ macrophages that were newly imported from the periphery, whereas “old” lesions lacked Mac387+ cells. / Thesis (BS) — Boston College, 2009. / Submitted to: Boston College. College of Arts and Sciences. / Discipline: College Honors Program. / Discipline: Biology.