Date of Award

5-2009

Document Type

Honors Thesis

Degree Name

Bachelor of Science

Department

Biological Science

Abstract

The acquired immune deficiency syndrome, AIDS, is a growing epidemic in the United States and the world. Since its discovery in 1981, the virus that causes AIDS, human immunodeficiency virus (HIV), has escalated. .Certain African ape (i.e., chimpanzees and gorillas) and monkey species are known to harbor forms of the virus termed SIV (simian immunodeficiency virus). Chimpanzees are the natural hosts of the SIV strains from which HIV-I evolved, but do not rapidly progress to AIDS, unlike their human relatives. In the wild, gorillas have been observed to harbor SIV, but this species' disease progression is currently unknown. As the closest living species to humans, the chimpanzee genome is over 95% identical to the human genorne, yet genetic differences between the species are known to exist that are thought to play a role in their different responses to SIV/HIV infection. It is posfulated that African apes and monkeys have co-evolved with SIV for a few million years, and thus have been able to adapt to, and co-evolve with, this deadly virus. By contrast, the recent cross-over of HIV to humans would suggest that such adaptive changes are missing from the human genome. Previous work by this and other labs has identified the T cell surface proteins CD4, CCR5, and CXCR4 which are involved in HIV infection of these cells potential targets of selection in the viral-host response. This past year I analyzed the protein-coding exons of the CD4, CCR5 and CXCR4 genes and their inferred proteins from a variety of primate species. In addition to the analysis of these host genes,I gathered numerous sequences for the F{IV/SIV surface protein gpl20 and scanned the translated amino acid sequences for unique changes at sites of interaction with the host CD4 protein. I found strong evidence for rapid evolution of CD4 on the chimpanzee hneage, and found no change on the human lineage. Two of the amino acid replacements on the chimpanzee lineage create two potential N-linked glycosylation sites which, if glycosylated, would likely interfere with gp120-binding. This finding supports the thesis that chimpanzees have adapted genetically to SIV.

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