Date of Award

5-2011

Document Type

Thesis

Abstract

Human immunodeficiency virus (HIV) is a virus that attacks the T helper cells, specifically the CD4 cells, in humans. CD4 cells are the cells that help fight infections in the body. Since HIV attacks the body's defense system, without treatment, the body gradually wears out and becomes unable to suppress virus replication. As healthy cell numbers dip lower, the body becomes immune compromised and more susceptible to other infections. HIV infections will progress into Acquired Immune Deficiency Syndrome (AIDS), which is ultimately fatal (see Hutchinson 2001) So why is it that despite the vast scientific knowledge about how the virus works, people around the world are still suffering from this disease in epidemic proportions? Biologically, the nature of the virus lends itself to high rates of mutation during replication. This, simply put, means a vaccine is exceptionally difficult to create (Hutchinson 2001). Drug treatments are available, and, if taken consistently and for the rest of one's life, can squelch virus replication a considerable amount, prolonging a patient's life. Unfortunately, these life-saving drugs are very expensive and often unattainable for people in developing nations. Additionally, poor adherence to the drug regimen can lead to drug-resistant viruses. Biology can only hold so much responsibility for the epidemic, though. In recent years researchers from a variety of backgrounds have studied and theorized why HIV/AIDS has continued to spread and among which populations. Social inequalities appear to be one the biggest explanations for why HIV/AIDS still persists and determinant of who will be infected.

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