Thesis advisor: Kenneth C. Williams / Individuals infected with Human Immunodeficiency Virus (HIV) are susceptible to pathological abnormalities due to the infiltration of virus into different anatomical compartments. Monocytes are a heterogeneous population that undergoes changes in phenotype with HIV infection. It is hypothesized that changes in monocyte subsets observed through the course of infection will correlate with the development of SIV-Encephalitis (SIVE). 14 CD8+ T cell depleted rhesus macaques were infected with SIVmac251 and changes in 3 monocyte subsets, defined by their CD14 and CD16 surface expression as CD14+CD16-, CD14+CD16+, and CD14-CD16+, were tracked through the course of disease. The CD14+CD16- subset increased in the absolute number of cells and decreased in percentage of the total monocyte population. The CD14+CD16+ and CD14-CD16+ subsets increased in both absolute number and percentage. These changes have a biphasic dynamic that occurs during early infection and is pronounced in encephalitic animals. Several markers showed differential expression with infection and between subsets. Mac387, an early monocyte-macrophage marker, demonstrated a considerable decrease in expression. Concomitant with this change, CD68, CD163, CD44v6, CCR2, and CD64 increased expression in the total monocyte population, with the magnitude of these changes occurring in a subset-specific manner. In conclusion, monocyte subsets undergo changes with SIV infection that correspond to the development of encephalitis, highlighting the contribution of monocytes in neuroAIDS. / Thesis (MS) — Boston College, 2010. / Submitted to: Boston College. Graduate School of Arts and Sciences. / Discipline: Biology.
Identifer | oai:union.ndltd.org:BOSTON/oai:dlib.bc.edu:bc-ir_101455 |
Date | January 2010 |
Creators | Shin, Hyunjin |
Publisher | Boston College |
Source Sets | Boston College |
Language | English |
Detected Language | English |
Type | Text, thesis |
Format | electronic, application/pdf |
Rights | Copyright is held by the author, with all rights reserved, unless otherwise noted. |
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