C-C Chemokine Receptor 5 and HIV: Therapeutic Potentials of the Delta 32 Base Pair Deletion

Presentation Type

Oral and/or Visual Presentation

Presenter Major(s)

Biomedical Sciences, Spanish

Mentor Information

Steven Hecht, hechts@gvsu.edu

Department

Biomedical Sciences

Location

Kirkhof Center 2263

Start Date

13-4-2011 1:00 PM

End Date

13-4-2011 1:30 PM

Keywords

Health, Illness, and Healing

Abstract

The Human Immunodeficiency Virus, a retrovirus discovered in 1981, has reached pandemic status worldwide. Without an existing cure or vaccine, a majority of the world's population remains at risk for infection and more than 35 million people to date have died from AIDS. Resistance to the virus, however, has been discovered in 10% of the world's population in the form of an allelic base pair deletion located on C-C chemokine receptor 5. Those homozygous for the base pair deletion are resistant to HIV while heterozygotes have displayed delayed onset of HIV infection. The CCR5 mutation and observed resistance to HIV in those bearing the base pair deletion represent exciting possibilities for the prevention and treatment of the virus. A new class of pharmaceuticals termed CCR5 antagonists, as well as CCR5-?32 stem cell transplantation, hold therapeutic promise not just for HIV but also other chemokine mediated diseases, including rheumatoid arthritis, autoimmune myocarditis, and cancer.

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Apr 13th, 1:00 PM Apr 13th, 1:30 PM

C-C Chemokine Receptor 5 and HIV: Therapeutic Potentials of the Delta 32 Base Pair Deletion

Kirkhof Center 2263

The Human Immunodeficiency Virus, a retrovirus discovered in 1981, has reached pandemic status worldwide. Without an existing cure or vaccine, a majority of the world's population remains at risk for infection and more than 35 million people to date have died from AIDS. Resistance to the virus, however, has been discovered in 10% of the world's population in the form of an allelic base pair deletion located on C-C chemokine receptor 5. Those homozygous for the base pair deletion are resistant to HIV while heterozygotes have displayed delayed onset of HIV infection. The CCR5 mutation and observed resistance to HIV in those bearing the base pair deletion represent exciting possibilities for the prevention and treatment of the virus. A new class of pharmaceuticals termed CCR5 antagonists, as well as CCR5-?32 stem cell transplantation, hold therapeutic promise not just for HIV but also other chemokine mediated diseases, including rheumatoid arthritis, autoimmune myocarditis, and cancer.