Medical Anthropology (Research Paper Sample)

HIV/AIDS
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The Etiology of HIV/AIDS
HIV/AIDS results from human Immunodeficiency Virus (HIV), the viral agent causing AIDS. The HIV enters the body through contact with blood and body fluids (Simon et al. 2006). When the virus enters the human host, it undergoes a life cycle that facilitates its growth and development within the human host. The HIV is enveloped and has a structure comprising if an outer lipid bilayer, an inner core having strands of RNA bound by a gag-like protein, p24, glycoproteins (Simon et al. 2006 p 492). These factors result in the infectivity and prognosis of the disease in the human host. The existence of these factors facilitates the infection and prognosis of the HIV.
The HIV infection commences with the attachment of the virus to the cell surface of a healthy human cell membrane. Simon et al. (2006) contend that the surface membranes of all living cells contain receptors through a ligand can attach to the cell. These receptors are specific for certain ligands, in what is commonly called stereospecificity or the lock and key analogy. The HIV is specific for two types of receptors in human beings; the CD+ cells and a secondary chemokine co-receptor like CCR5 or CXCR4. As a result, through binding of the virus to its specific receptors found on the membrane surface, and then other proteins that facilitate a tight fusion between the viral particles and the receptors are activated.
Once the virus binds to the human cell, its core and associated particulate RNA enter the cell (Simon et al. 2006 p. 492). The virus has a nucleocapsid to facilitate its evasion from the host's defensive network. As soon as enters the human cell, the protective envelope dissolves, facilitating the commencement of the viral replication and the infective process. The dissolution of the nucleocapsid results in the release of the genetic material to the cell's cytoplasm of the human cell. The release facilitates the conversion of the viral RNA to DNA, in an enzymatic process. The enzyme commonly involved is the RNA-specific reverse transcriptase enzyme. The enzyme is secreted by the HIV virus and is released into the host cell's cytoplasm where it actively transcribes the RNA into DNA. In drug development and design, this enzyme is usually targeted in a bid to reduce the viral latency within the human cell. Furthermore, there is a consensus among researchers that the step involving the reverse transcriptase enzyme is error-prone, often resulting in extreme heterogeneity of the virus. As a result, some mutations are serially introduced into the virus every time it undergoes replication. This makes it hard to develop effective anti-effective agents for the virus.
After the virus has completed its replication cycle, the resultant viral DNA gets inserted into the host cell DNA with the aid of the viral integrase enzyme (Simon et al. 2006). The involvement of the integrase enzyme in the viral cycle has made it possible for the development of drugs that target the integrase enzyme, as part of the fight against HIV/AIDS. Once the viral DNA attaches to the human DNA, the former may remain in a non-infective state for many years without the host knowing of the presence of the virus in their system. When HIV latency occurs, its diagnosis and prevention becomes extremely impossible, hence, the challenges that come with HIV eradication or treatment.
The activation of the virus-laden host cells results in the transcription of the viral DNA in the host cell alongside the DNA of the host into messenger RNA (mRNA) (Simon et al. 2006 p. 494). The new viral RNA serves as a template for the synthesis of other viral genetic particles in a repetitive cycle that sees the exponential multiplication of the virus. According to Simon et al. (2006), some of the transcribed viral mRNA is translated to produce protein and enzymes that facilitate the continuity of the cycle, and the spread of the viral infectivity to other non-infected cells. After its formation in the nucleus, the mRNA is transported outside of the nucleus into the cytoplasm of the human cell. As a result, the translational particles such as the viral proteins and enzymes form the foundation for the construction of the new HIV particles.
The viral cycle does not stop at the formation of the proteins and enzymes. After the assembly of the new virion particles, while functional proteins then follow. The functional viral proteins are mainly the envelope and the core proteins, which include the Gag, the gp 120, and the gp41 (Simon et al. 2006 p. 492). Furthermore, the virus also secretes enzymes such the reverse transcriptase, integrase and protease as part of its assembly. When the viral RNA and its particulate matter are assembled and packaged in the cytoplasm, they "pinch off" small portions of the host membrane to form an envelope that protects from the host's immunity. Simon et al. (2006 p. 496) contend that the "pinching" action of the viral particle results in the eventual destruction of the cell, and if it occurs in the CD4+ cells, then the host becomes highly immunocompromised. This stage presents myriad clinical manifestations of HIV/AIDS. As a result, the maturation of the virus facilitates the rapidity of infection and the destruction of the CD4+ cells that aid in the defence against the pathogenic micro-organisms.
The Epidemiology of HIV/AIDS
The HIV/AIDS is considered a global pandemic, owing to its multi-border occurrences. According to WHO (2013), since the beginning of the epidemic in 1981, close to 78 million people have been infected with the virus as of 2013, while about 39 million have died. Globally, close to 35 million people were living with HIV by the end of 2013, with 0.8 percent of the victims being adults aged 15-19 years. The burden of the infection varies differently across continental and regional divides. Sub-Saharan Africa strikes as a region with the highest prevalence and incidence of the disease, where nearly 1 in every 20 adults has the disease. As a result, the huge prevalence of the infection in Africa accounts for close to 70% of the disease burden in the world. As a result, AIDS becomes the leading cause of premature death among 15-59-year-old individuals, creating a socio-economic crisis in the affected countries.
Merson (2006) reports that the first incidences of HIV/AIDS occurred among five homosexual men as at June 1981. However, from that time onwards, the disease has continued to widen its scope of fatalities, killing millions in the process. The epidemiology is supported by Simon et al. (2006) who contend that in 2005 alone, there were 4.1 million new HIV-reported cases, with 2.8 million of them dying in the process. In the United States, close to one million Americans were living with the disease in 2008, while new incidences reached over one million in 2011. In the United Kingdom, the Public Health England (PHE) (2014) reports that close to 107800 people were living with HIV/AIDS as of 2013. An estimated prevalence of 2.8% occurs in the population aged 15-59 years in every 1000 individuals. According to the PHE (2014), approximately 6000 persons were diagnosed with HIV in 2013, with 320 of them developing AIDS. The consequences of the pandemic on the population is significantly undesirable. Deaths arising from the disease result in labour deficits, economic challenges and family disruptions. The family disruptions emanate from the absence of one or all of the parents, leading to disruptive growth among their children.
The Ecological/Evolutionary Model and the Epidemiology of HIV/AIDS
The ecological/evolutionary model conceptualises the disease process regarding the "micro-organism," the "host," and the "environment" (Joralemon, 2015 p. 37), forming an epidemiological triangle. The environment alludes to the setting in which the disease occurs, whether physical, socio-cultural, or the climatic. Applying this model to the HIV/AIDS pandemic, the disease is caused by the HIV.
From the micro-organism’s perspectives, the HIV's process of reverse transcription is error-prone, allowing small amounts of mutations to be introduced every time the virus replicates (Simon et al. 2006 p. 493). The mutation results in extreme heterogeneity of the virus, which makes it hard to target using anti-retroviral therapy. Furthermore, the ability of the virus to remain in latency after the formation of the virion particles makes it hard to diagnose, prevent, or treat the disease. As Joralemon (2015 p. 36) observes, the possession of such abilities confers a selective advantage to the HIV, allowing them to destroy the host's immunity and the anti-retroviral therapy. The HIV has two serotypes; HIV-1 and HIV-2, which also have smaller subtypes that show morphological differences. The existence of the serotypes and the incidences of viral mutations may be the reason the disease continues to be a global pandemic despite the existing controls to prevent and treat it.
From the host perspectives, individual characteristics are likely to predispose the host to HIV/AIDS. Factors such as race, ethnicity, personality, gender, sexual orientation, and the socio-economic position have been shown to predispose an individual to HIV/AIDS. According to PHE (2014), an individual’s sexual orientation has been largely attributed to the spread of HIV. In the UK for instance, men who have sex with other men (MSMs) remain the group most at risk of contracting the virus. In 2013 alone, there were 3250 new HIV diagnoses reported among the MSMs. The number is slightly higher compared to the new to the new diagnoses of 3230 in 2012. As a result, in the UK, the new Diagnoses of HIV in MSMs account for 54% of all infections in the country. Similarly, in the US, Pellowski et al. (2013) report that MSMs demonstrate a slightly higher i...