Human Immunodeficiency Virus ( Hiv ) Essay

Human Immunodeficiency Virus ( Hiv ) Essay

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My group and I choose human immunodeficiency virus (HIV) as our organism to explore evolutionarily. Our organism, HIV is retrovirus that infects human beings of every religion, color or creed. HIV can result in profound viremia and low T-cell counts characterized as acquired immune deficiency syndrome (AIDS). HIV first appeared in the 1980’s largely in males practicing anal receptive sexual behavior; HIV had not yet been characterized however medical personnel noted that this population had stubborn infections that were resistant to most medication. Today, we understand these individuals were suffering from HIV/AIDS and were actually immunodeficient. It is postulated that both strains of HIV descend from simian immunodeficiency virus (SIV) a virus that infects non- human primates. In this paper we will explore the evolution of HIV resistance and the mutations that lead to slower disease progression.
All viruses such as HIV are composed of three main components namely genetic material, a protein coat and an envelope. HIV is a spherical structure measuring about 0.1microns in diameter. It belongs to the family Retrovirus, sub classified as a Lentivirus, which has a prolonged incubation period. HIV is an enveloped virus containing two positive single stranded (+SS) RNA. The HIV envelope has special proteins moieties called glycoprotein 120 (Gp 120) and glycoprotein 41 (Gp 41), coded for by the env gene, that aid in cell fusion and entry.
For our discussion it is important to define the special protein receptors that HIV needs in order to enter cells. They are the envelope protein Gp 120 binds to cluster of differentiation 4 (CD 4) and associated chemokine receptor 5 (CCR5/ CD195), a co-receptor used to facilitate fusion and entry. ...


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... of the CCR5 D32 mutation is still up for debate but “has been found in skeletal remains about 2,900 years old (Hummel et al. 2005)” which means the mutation may very well be older than 2900 years. The population with the highest frequency is Europe at about 10% on average carrying this CCR5 D32 mutation, suggesting it bears a selective advantage and that genetic drift is not plausible as previously suggested. The CCR5 D32 mutation demonstrates its greatest prevalence in Scandinavian countries, where smallpox epidemics hit intensively in the past (Galvani and Slatkin 2003). Bauduer’s suggested a link between the small pox outbreak and the CCR5 D32 mutation in the European population, this single paper doesn’t provide definitive evidence but it does support the theory. We are one step closer to creating a plausible timeline of the development of the CCR5 D32 mutation.

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