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The REAL Origin of HIV/AIDS: USA Infected Africa and the Rest of the World with HIV/AIDS?

Africa

Acquired Immunodeficiency Deficiency Syndrome (AIDS) at one point in time, became a death sentence for most infected people living in less developed countries in the world (Kapstein and Busby, 2013). The unannounced and unpredicted rapid emergence and spread of this slow acting viral infection baffled many including well known scientific bodies such as the World Health Organisation (WHO). This essay is going to research into and propose the probable origin of this disease as in relation to historical incidents, coupled with both popular and unpopular scientific theories about it.

AIDS is believed to be caused by the effect of the human immunodeficiency virus (HIV). Furthermore, AIDS is terminology used to describe a range of diseases and infections which are present in people with a weakened immune system caused by HIV. In other words, AIDS is the late stage manifestation of HIV (Kenny et al, 2012).

HIV is a retrovirus, as such, it uses its single stranded ribose nucleic acid (RNA) to make copies of deoxyribose nucleic acid (DNA) inside a host cell; in this case a lymphocyte called T lymphocyte helper cell with CD4 receptors on its surface membrane (Whiteet al, 2011). When the HIV enters the cytoplasm of a T helper cell with CD4 receptor, also known as CD4 T lymphocyte cell, it employs an enzyme called reverse transcriptase which produces DNA from the virus RNA. This is the reverse of the transcription process whereby DNA is used to produce a strand of RNA for protein synthesis. The newly produced DNA strand is then replicated to form two strands of DNA held together by a weak bond.

The DNA strands move into the nucleus and then integrated into the genetic material (genome) the host CD4 T lymphocyte cell using a retroviral integrase enzyme (Krebs et al, 2014). The HIV genetic material becomes part of the chromosome of the CD4 T lymphocyte cell and either stays dormant or virus RNA will be produced from the virus DNA to make proteins necessary for new viruses. When the new viruses are formed, they burst out of the CD4 T lymphocyte cells to infect other CD4 Tlymphocyte cells, repeating the same process over again (Alberts et al., 2013).

The HIV causes the destruction of CD4 T cells via cellular mechanism such as apoptosis of surrounding cells, killing of infected CD4 T lymphocyte cells when newly formed viruses burst out of the cell and the killing of infected CD4 T lymphocyte cells by cytotoxic lymphocyteswith a chemical called perforin (Garg, Mohl and Joshi, 2012; Kumar et al., 2012). HIV easily compromises the immune system of humans because it targets the lymphocytes which are necessary in the defence against pathogens; it attacks the cells which are supposed to protect the human body from disease causing foreign cells (Sompayrac, 2012).

According to the classification system introduced by the Centers for Disease Control and prevention (CDC) of the United States, there are various stages in HIV infection symptom manifestation (Curran and Jaffe, 2011).

Stage I, also known as the acute seroconversion illness, begins between one and six weeks after the patient is infected with the virus. Typical symptoms of this stage include fever, enlarged lymph nodes (lymphadenopathy), persistent headaches, and diarrhoea. At this stage, the HIV infection treatment with antiretroviral therapy (ART) has a higher rate of success than any stage therefore highlighting the importance of early diagnosis (Weeks and Alcamo, 2010).

At this stage, the number of virus in the body system fluctuates due to an increased in the transcription of virus RNA and subsequent production of the virus in the CD4 T lymphocyte cells of the immune system. The capacity to transmit the virus is extremely high at this stage due to the elevated levels of the virus in the body. The immune system gradually lowers the number of the virus in the body to a normalised level due to the increase in the production of more CD4 T lymphocyte cells (CDC, 2014).

Stage II also known as the asymptomatic stage, at this stage, even though HIV is still and reproducing at a slow rate, no symptoms are exhibited by the host. The host body will not manifest any infection for periods which could last for more than a decade for some patients but shorter for others. Towards the end of this stage, the level of HIV in the host begins to rise as the level of CD4 T lymphocyte cells begin to fall.

As this commences, the patient will begin to manifest HIV related infections as the immune system becomes compromised. Persistent generalised lymphodenophthy (PGL) begins to manifest for three or more months. Even though virus level may seem to be low, the ability to transmit the infection remains potent however lower in patients receiving ART. This is the early stages of the last stage of the HIV infection; AIDS (Greenwood et al., 2012).

The last stage (AIDS) is characterised by a severely damaged immune system which leads to its inability to offer any method of defence to infections and infection related tumours called opportunistic infections. There are two determinant factors in AIDS. The first one is when the CD4 Tlymphocyte cells level falls below 200 cells per microliter of blood. The average level of CD4 T lymphocyte cells is around 500 to 1600 per microliter.

The other determinant factor is a patient developing one of more opportunistic infection, which has no relation to the level of CD4 T lymphocyte cellsin the blood of the host. Opportunistic infections include pnuemocystiscarinii which causes fever, pain in the chest, tiredness and fatigue, bacterial infections such as tuberculosis, which is more prevalent in developing countries with traces of the disease within the population, mycobacterium avium complex is more prevalent in HIV patients in industrialised countries characterised by night sweating, diarrhoea, pains in the abdomen and weight loss. Kaposi’s sarcoma, a tumour which affects the lungs and digestive track causes the shortness of breath, coughing of blood, pains in the abdomen or bleeding (Shields and Shields, 2008).

Modes of transmission of HIV involve the exchange of bodily fluids between an infected person and a healthy person. In an infected patient, HIV count is highest in the blood, semen and vaginal fluid (Ramaiah, 2008). HIV is transmitted through either horizontally or vertically. Horizontal transmission includes infections acquired via sex (between men and women, also known as heterosexual sex, sex between men), use of contaminated needles for intravenous drug usage and transfusion or exchange of contaminated blood products. Vertical transmission is the transmission of the virus from mother to child (Wellensiek, 2007).

Transmission of HIV is most common with sexual contact with an infected person. Globally, a major method of transmitting is via sex between men and women. Nonetheless, this is significantly different among countries with different economic status. In the United States, men who engage in homosexual contact account for about 64% of newly infected people (CDC, 2014b). Whereas, in the United Kingdom heterosexual unprotected sexual intercourse transmission has overlapped homosexual intercoursetransmission (Thomas and Willacy, 2011). More so, studies reveal a negative correlation between the economic status of a country and the level of transmission risk through unprotected sex. The risk of transmission is about four to ten times more in developing countries than in developed countries (Boily et al., 2009).

Blood and blood products represent the second most common mode of transmission for HIV (Rom and Markowitz, 2007). This mode can occur via transfusion of infected blood, intravenous drug usage with shared needle and contaminated needle injury. The transmission rate for HIV with infected blood is about 93%. The risk of getting infected with HIV in developed countries is very low, however, in developing countries blood transfusion with infected blood represents about 15% of HIV infections (Rom and Markowitz, 2007). In the United States, needle sharing by drug users represent over 10% of newly infected patients in 2009 alone. Furthermore in some areas over 80% of intravenous drug users are infected with HIV (Rom and Markowitz, 2007).

Mother to child transmission occurs during foetus development, child birth, or during breastfeeding. The risk of HIV transmission through mother-to-child is about 20% at child birth and 35% during breastfeeding of babies (Coutsoudis, Kwaan and Thomson, 2010). Furthermore, mother-to-child transmission represents about 90% of HIV infection in children (Coutsoudis, Kwaan and Thomson, 2010).

Currently there is no cure or vaccine for HIV; however, there are two methods of treatment for people infected with HIV; antiviral therapy and medication for opportunistic infections.

Antiviral therapy involves the use of antiretroviral medications to retard the reproduction of HIV in the body. There are six classes of antiretroviral drugs; non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors, CCR5 antagonists and integrase inhibitors. These drugs work in different ways such as nucleoside reverse transcriptase inhibitors prevent the virus RNA from being reverse transcribed by the DNA polymerase in the nucleus of the CD4 lymphocyte cells (Ka’opua and Linsk, 2007). The medications are administered in combinations to increase its efficacy (WHO, 2014). In order to reduce the risk of death, the World Health Organisation recommends the commencing of antiretroviral drug treatment when the CD4 T lymphocyte cell count falls below 350 per microlitre of when people exhibit symptoms of the disease.

The prevention of opportunistic infections helps greatly in the management of the disease. The administration of antiretroviral medication proves effective at reducing the chances of developing opportunistic infection since virus reproduction is slowed down therefore the CD4 T lymphocyte cells count rises to maintain the functionality of the immune system (Montessori et al., 2004). A combination of antibiotic medications such as pneumocystic pneumonia (PCP) and vaccination for hepatitis A and B are also administered to people with high risk of developing HIV or those who are newly diagnosed (Laurence, 2006). Prophylaxis medications combined with antiretroviral drugs and cessation of breastfeeding successfully reduces the risk of vertical transmission of the infection to a baby. However, some antiretroviral medications cause birth defects therefore are not given to HIV infected women who want to give birth or are already pregnant.

Preventive measures employed to stop the spread of HIV infection includes the promotion of the awareness of the disease, safer sex lifestyle, use of new needles by drug users, and the use of pre-exposure and post-exposure prophylaxis.

Safe sex practices such as the consistent use of condoms with multiple sex partners and the reduction of promiscuity. Regular usage of condoms over a long period reduces the chances of transmission by about 80%, the rate of transmission between an infected person and the partner is about 1% per year if condoms are used regularly according to the WHO (Crosby and Bounse, 2012). The use of reverse transcriptase inhibitor as soon after sexual intercourse by women has been shown to provide some success at preventing transmission. However, evidence proves that the use of abstinence as a preventive measure has been unsuccessful at reducing the spread of the disease (Underhill, Operario and Montgomery, 2007).

Transmission caused by needle-sharing by intravenous drug users has been reduces drastically by programmes such as need-exchange schemes.

Pre-exposure prophylaxis such as antiretroviral administration of tenofovir to infected people with CD4 T lymphocyte cell counts below 340 per microlitre provides 96% protection for their partners from getting infected (Anglemyer et al., 2011).

Post-exposure prophylaxis like zidovudine with tenofovir or other antiretroviral medications has been documented to decrease the risk of getting infected through needle injury by about five folds (Kuhar et al., 2013).

HIV is a chronic disease, therefore without the onset of the AIDS, the prognosis of patients is between nine to eleven years without treatment (UNAIDS and WHO, 2007). After the onset of AIDS, the person can survive up to 19 months without any treatment (Vogel et al., 2010). Antiretroviral medication and medications against opportunistic infections early administration increases the survival and life expectancy of HIV patients to about 20 – 50 years. However, when disease management through antiretroviral treatments are started after the development of AIDS, the life expectancy of the patient is reduced by as much as 10 years (Vogel et al., 2010).

The origin of HIV, as of now, remains unknown because there is no fact to support theories which seek to offer an origin to this epidemic. However the average person believes only the popular theories out of the numerous ones due to the influence of media attention and popularisation of these theories more than others (Poku, 2005).

The most popular theory in the origin of HIV is the hunter theory. In this theory, it is believed that Simian Immunodeficiency Virus (SIV) which shares some similarities with HIV was transferred to humans from chimpanzees being killed via the process of butchering the meat or a hunter being bitten by the animal (Jenkins, 2009). According to scientists who support this theory, under normal circumstances, the human immune system is able to fight off this viral infection. However, at some point in time, the virus could have mutated its genetic material to become the modern HIV virus which causes AIDS (Condon and Sinha, 2008).

This theory furthermore suggests that during 1950s health professionals in some African countries due to lack or limited supply of disposable syringes may have used one syringe to inject multiple patients without stringently sterilising it. This therefore made it possible for the SIV to be transferred to numerous unsuspecting people, making it effortless for the SIV to mutate to become HIV (Hoerl and Neidermeyer, 2009). Wolfe et al (2004) conducted a study revealed that 1% of 1099 individuals who are reported to have come into contact with blood and body fluids of non-human primates, have immune system antibodies to simian foamy virus (SFV), a retrovirus found in old world primates. This finding suggested that the 1% of the samples had been infected with the SFV but their immune system successfully fought off the virus.

This single study was highly publicised which resulted in people calling for the ban on the consumption of non-human primates so as to curb the transmission of animal infection to humans (zoonotic infection). However, this study does not directly give evidence of modern occurrence of zoonotic infection. Even though SFV is a type of retrovirus, there was not one case of the virus mutating into becoming HIV. Also, out of the 1099 samples used, even though it is documented they were in contact with non-human primates blood (the main origin of HIV according to this theory), none of the samples had any strain of SIV when then mutated into HIV, even though it is believed to be prevalent in about 35% of non-human primates in central Africa (Mahy and Van Regenmortel, 2010). Furthermore, hunting non-human primates as food has been practiced for several millennia in the continent of Africa, therefore for SIV mutation to HIV to emerge only in the 20th century to become a pandemic just under a century comes as an unlikely explanation (Jenkins, 2009).

Another supporter of the hunter theory is the colonialism theory suggested by Jim Moore, a primate behaviour specialist. Moore, in his findings report, suggested that during late 1800s and early 1900s, most the African continent was under European colonial rule. Countries like Congo and some central African colonies experienced crude and savage treatment from colonial European countries like Belgium. Natives were forced into hard labour camps with poor nutrition, sanitation and health care provision. This, according to Moore, provided a conducively weak immune system for SIV to mutate into becoming HIV.

Another factor was the likelihood for the hungry labourers to perhaps hunt down a sick chimpanzee to be used as a rare protein treat and also the Moore stipulates the camps used prostitutes to make the workers happy, therefore increasing the possibilities of transmitting the disease. In addition, it is likely immunisation of the workers would have been with shared unsterilized syringes (Chitnis, Rawls and Moore, 2000). However, even if the scenario of this theory is true, it is highly unlikely for a labour to live long enough for the disease to advance into AIDS. Furthermore there are no records, including medical records, of the existence of the camps to support this theory. 50% of the population of the camps in Congo were killed, therefore, to cover up this act records of the camps were destroyed (Jenkins, 2009).

An unpopular theory which has not received attention both from the media and scientific bodies is the vaccine hypothesis proposed by Dr Gerald Myers, head of HIV sequence database at Los Alamos National Laboratory in New Mexico, regarded as a pioneer in the study of HIV evolution (Connor, 1995). Myers and colleagues, in their study of the HIV genetic material sequence, concluded that the origin of HIV could not have been as proposed by the hunter theory or any other isolated zoonotic infection.

They furthermore pointed out that evidence from the genetic sequence of HIV studies proved that an incident occurred during the mid-1970s triggered the evolution of different subtype strains of HIV (Burr, Hyman and Myers, 2001). Myers and his colleagues employed a forward-processed simulation and coalescent theory to determine whether the emergence of subtypes of HIV was as a result of natural evolution influenced by environmental factors which results in survival traits being preserved, in this case the host or not. Their conclusion from the simulation revealed that HIV evolution was not comparable to the evolution of a very similar virus (feline immonodeficiency virus).

This resulted in their assertion that the evolution of HIV is of not any natural Darwinian evolution, however it is most likely caused by Lamarckian evolution whereby traits are passed on to offspring by parent organism. In summary, Myers and his colleagues through their simulation revealed the development of HIV subtypes are as a results of the parent virus transferring inheritable traits to the offspring, contrary to the zoonotic infection theories.

Horowitz (1996) with his research of scientific documents and National Institutes of Health contracts provides support for Myer’s proposition by suggesting that chimpanzees contaminated with various virus were used to cultivate hepatitis B vaccines which were administrated to central African natives and homosexual males in New York. Horowitz highlighted the same period proposed by Myers as when a trigger was given to the HIV evolution (1970s). Horowitz suggested that HIV was either intentionally or accidentally introduced into research chimpanzees which resulted in the presence of the virus in the vaccines made from those chimpanzees. Horowitz’s preposition of contamination of vaccines with disease causing pathogens holds credibility, according to certain historical incidents through history.

The suggestion of organisations such as the USA government creating a disease such as HIV to infest a certain part of the population may sound up surd to everyone in this modern age, however, it is worth noting that the Tuskegee Syphilis experiment at one point seemed equally farfetched until it was revealed to have really happened under the supervision of the United States’ Public Health Services (Jones, 1993). Furthermore, recent revelations have reinforced the vaccine theory as a very probable explanation for the origin of HIV. In 2009, Baxter healthcare, a US company produced vaccines which received approvals from the USA and EU regulators to be given to people.

However, when Czech Republic researchers introduced the vaccines to ferrets, they got infected with deadly avian flu (Moritz, 2011). Baxter, in their defence claimed the vaccine was accidentally contaminated with avian flu, however, the chances of a multi-billion dollar company with strict safety implementation to let a contaminated vaccine slip through to customers is a hard to believe incident. Furthermore, it was only by chance that the Czech researchers found the contamination out, if this had not been found, people would have been infected with this deadly virus same way as HIV, according to Horowitz (Horowitz, 1996).

A front page article in The Times cited an unnamed WHO executive who revealed that evidence points to the activation of HIV or possibly the mutation of SIV to HIV by the live smallpox vaccines (vaccinia) given to people (Appendix B). In this article, the Walter Reed Army Centre in Washington is reported to have documented a 19 year old recruit, who after receiving vaccinia, exhibited AIDS related symptoms and died shortly.

The article furthermore highlighted a trend, whereby countries that received more smallpox vaccine recorded high rates of HIV. The most intense immunisation programmes took place in Zaire (DR Congo), Zambia, Tanzania, Uganda, Malawi, Rwanda and Burundi, in descending order. Furthermore, the leading central African country with the highest cases of HIV infection is Zaire. In addition, Brazil, the only South American country which took part in the smallpox immunisation, interestingly, has the highest cases of HIV in that region (Pearce, 1987).

Even though the real figures of HIV infection people in Africa are not readily available, Pearce (1987) points out those countries with the highest number of cases are the same countries which undertook intensive smallpox vaccination under the supervision of the WHO.

Julian Cribb, a fellow of the Royal Society of London, protested about how very little attention is given to unpopular scientific explanations with factual evidence, by main stream science journals and the media (Cribb, 2001). Cribb highlighted the lack of interest by scientist to investigate and promote hypothesis that has any possibility to prove the origin of HIV being in an accident by a scientific body. Evidently, efforts have been attempted to falsify the existence of HIV prior to the period cited by this theory (Connor, 1995).

However, smallpox is now regarded as a contraindication of HIV, according to some studies into the side effects of smallpox vaccine (Maurer, Harrington and Lane, 2003). Furthermore, the news article has been criticised for lacking a credible name to its revelations. Some articles, in addition, suggest smallpox vaccination helped in the fight against HIV (Conor, 2010). However, this study was performed in a laboratory test tube therefore lack any comparative credibility to real life situation. Furthermore, any change made to the vaccinia virus used in the vaccine was not noted apart from the name of the vaccine.

The origin of HIV still remains unknown, even though a lot of efforts has been put into unearthing the factual truth. However, it is unfortunate the science society, especially, has not given attention to every theory but stubbornly only seem to accept the zoonotic infection theories than any other theory (Horowitz, 1996). As a body that deals with facts and open minded to ideas as long as they offer valid measurable and reliable evidence, it is quite surprising perspectives which seem to unearth mistakes undertaken by reputable scientific bodies are not given the necessary platform.

The move by major scientific bodies and mainstream media not to give attention to unpopular but viable theories of the origin of the disease increases the number of people who mistrusts these bodies. Even though the reputation of that body is at risk of being damaged by such theories, it would motivate other bodies to be very dexterous with their works, only produce materials which are safe and harbour no unknown detrimental side effects or accidents.

However, it is relevant to point out that the knowledge of the true origin of HIV, as of now, offers no positive contribution to race to find an effective vaccine for the disease. Efforts made by mainstream scientific bodies and media have helped in the intervention of preventive measures and curb further spread of this disease. It is inherent that opposing theories and scientists are all focused on the eradication of the disease; therefore more efforts should be channelled towards that unifying goal.

References

Alberts, B., Bray, D., Lewis, J., Raff, M., Roberts, K., Hopkin, K., Johnson, A. and Walter, P. (2013).Essential cell biology. 4th ed. New York: Garland Science.

Anglemyer, A., Rutherford, G., Baggaley, R., Egger, M. and Siegfried, N. (2011). Antiretroviral therapy for prevention of HIV transmission in HIV-discordant couples. Cochrane Database of Systematic Reviews. [online] Available at: http://dx.doi.org/10.1002/14651858.cd009153.pub2 [Accessed 3 Jun. 2014].

Baggaley, R., White, R. and Boily, M. (2008).Systematic review of orogenital HIV-1 transmission probabilities. International Journal of Epidemiology, [online] 37(6), pp.1255-1265. Available at: http://dx.doi.org/10.1093/ije/dyn151 [Accessed 1 Jun. 2014].

Boily, M., Baggaley, R., Wang, L., Masse, B., White, R., Hayes, R. and Alary, M. (2009). Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies. The Lancet infectious diseases, 9(2), pp.118–129.

Burr, T., Hyman, J. and Myers, G. (2001). The origin of acquired immune deficiency syndrome: Darwinian or Lamarckian?. Philosophical Transactions of the Royal Society B: Biological Sciences, [online] 356(1410), pp.877-887. Available at: http://dx.doi.org/10.1098/rstb.2001.0864 [Accessed 3 Jun. 2014].

CDC, (2014). CDC – What is HIV/AIDS? – HIV Basics – HIV/AIDS. [online] Available at: http://www.cdc.gov/hiv/basics/whatishiv.html [Accessed 31 May. 2014].

 CDC, (2014b). CDC – Fact Sheet – Gay and Bisexual Men – Gender – Risk – HIV/AIDS. [online] Available at: http://www.cdc.gov/hiv/risk/gender/msm/facts/index.html [Accessed 1 Jun. 2014].

 Chitnis, A., Rawls, D. and Moore, J. (2000). Origin of HIV Type 1 in Colonial French Equatorial Africa?. AIDS Research and Human Retroviruses, [online] 16(1), pp.5-8. Available at: http://dx.doi.org/10.1089/088922200309548 [Accessed 3 Jun. 2014].

Condon, B. and Sinha, T. (2008). Global lessons from the AIDS pandemic. 1st ed. Berlin: Springer.

Connor, S. (1995). How scientists discovered false evidence on the world’s. [online] The Independent. Available at: http://www.independent.co.uk/news/uk/how-scientists-discovered-false-evidence-on-the-worlds-first-aids-victim-1612471.html [Accessed 3 Jun. 2014].

Conor, S. (2010). Smallpox vaccine ‘helped fight HIV’. [online] The Independent. Available at: http://www.independent.co.uk/life-style/health-and-families/health-news/smallpox-vaccine-helped-fight-hiv-1976451.html [Accessed 3 Jun. 2014].

Coovadia, H. (2004). Antiretroviral agents—how best to protect infants from HIV and save their mothers from AIDS. New England Journal of Medicine, 351(3), pp.289–292.

Coutsoudis, A., Kwaan, L. and Thomson, M. (2010).Prevention of vertical transmission of HIV-1 in resource-limited settings. Expert Review of Anti-infective Therapy, [online] 8(10), pp.1163-1175. Available at: http://dx.doi.org/10.1586/eri.10.94 [Accessed 1 Jun. 2014].

Cribb, J. (2001). The origin of acquired immune deficiency syndrome: can science afford to ignore it?. Philosophical Transactions of the Royal Society B: Biological Sciences, [online] 356(1410), pp.935-938. Available at: http://dx.doi.org/10.1098/rstb.2001.0878 [Accessed 3 Jun. 2014].

Crosby, R. and Bounse, S. (2012). Condom effectiveness: where are we now?. Sexual Health, [online] 9(1), p.10. Available at: http://dx.doi.org/10.1071/sh11036 [Accessed 3 Jun. 2014].

Cunha, B. (2012). Antibiotic essentials 2012. 1st ed. Sudbury: Jones and Bartlett Publishers, Inc.

Curran, J. and Jaffe, H. (2011). AIDS: the early years and CDC’s response. MMWR SurveillSumm, 60(Suppl 4), pp.64–9.

Dosekun, O. and Fox, J. (2010). “An overview of the relative risks of different sexual behaviours on HIV transmission.”. Current opinion in HIV and AIDS 5 (4): 291–7. doi:10.1097/COH.0b013e32833a88a3. PMID 20543603.

Garg, H., Mohl, J. and Joshi, A. (2012). HIV-1 induced bystander apoptosis. Viruses, 4(11), pp.3020–3043.

Greenwood, D., Slack, R., Barer, M. and Irving, W. (2012). Medical microbiology. 18th ed. Edinburgh: Churchill Livingstone/Elsevier.

Hoerl, R. and Neidermeyer, P. (2009). Use what you have. 1st ed. Bloomington: Xlibris Corporation.

Horowitz, L. (1996). Emerging viruses. 1st ed. Rockport, MA: Tetrahedron.

Jenkins, S. (2009). AIDS. Bloomington: AuthorHouse.

Jones, J. (1993). Bad blood. New York: Free Press.

Ka’opua, L. and Linsk, N. (2007). HIV treatment adherence. 1st ed. [Binghamton, NY]: Haworth Press.

Kapstein. E, Busby. J, (2013) AIDS Drugs for All. Cambridge: Cambridge University Press.

Kenny, T., Knott, L. and Cox, J. (2012).HIV and AIDS.Symptoms and Treatment | Patient.co.uk. [online] Patient.co.uk. Available at: http://www.patient.co.uk/health/hiv-and-aids [Accessed 28 Apr. 2014].

Krebs, J., Lewin, B., Kilpatrick, S. and Goldstein, E. (2014).Lewin’s genes XI.Burlington, Mass.: Jones & Bartlett Learning.

Kripke, C. (2007). Antiretroviral prophylaxis for occupational exposure to HIV. American family physician, 76(3), p.375.

Kuhar, D., Henderson, D., Struble, K., Heneine, W., Thomas, V., Cheever, L., Gomaa, A. and Panlilio, A. (2013). Updated US Public Health Service Guidelines for the Management of Occupational Exposures to Human Immunodeficiency Virus and Recommendations for Postexposure Prophylaxis. Infection Control and Hospital Epidemiology, [online] 34(9), pp.875-892. Available at: http://dx.doi.org/10.1086/672271 [Accessed 3 Jun. 2014].

Kumar, V., Abbas, A., Aster, J. and Robbins, S. (2012). Robbins basic pathology. 9th ed. Philadelphia, PA: Elsevier/Saunders.

Laurence, J. (2006). Hepatitis A and B virus immunization in HIV-infected persons. The AIDS reader, 16(1), p.15.

Mahy, B. and Van Regenmortel, M. (2010). Desk encyclopedia of human and medical virology. 1st ed. Oxford: Academic.

Maurer, D., Harrington, B. and Lane, J. (2003). Smallpox vaccine: contraindications, administration, and adverse reactions. American family physician, 68(5), pp.889–906.

Montessori, V., Press, N., Harris, M., Akagi, L. and Montaner, J. (2004).Adverse effects of antiretroviral therapy for HIV infection. Canadian Medical Association Journal, 170(2), pp.229–238.

Moritz, A. (2011). Vaccine-nation. Brevard: Ener-Chi Wellness Press.

Poku, N. (2005). AIDS in Africa. 1st ed. Cambridge, UK: Polity.

Rom, W. and Markowitz, S. (2007). Environmental and occupational medicine. 4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.

Shields, J. and Shields, C. (2008). Eyelid, conjunctival, and orbital tumors. 2nd ed. Philadelphia: Lippincott Wiliams& Wilkins.

Smith, D., Grohskopf, L., Black, R., Auerbach, J., Veronese, F., Struble, K., Cheever, L., Johnson, M., Paxton, L., Onorato, I. and others, (2005). Antiretroviral postexposure prophylaxis after sexual, injection-drug use, or other nonoccupational exposure to HIV in the United States: recommendations from the US Department of Health and Human Services. MMWR Recomm Rep, 54(RR-2), pp.1–20.

Sompayrac, L. (2012). How the immune system works. Chicester: Wiley-Blackwell.

Thomas, H. and Willacy, H. (2011). Acquired Immune Deficiency Syndrome (AIDS) | Doctor | Patient.co.uk. [online] Patient.co.uk. Available at: http://www.patient.co.uk/doctor/acquired-immune-deficiency-syndrome-aids [Accessed 1 Jun. 2014].

UNAIDS, and WHO, (2007). AIDS epidemic update. 1st ed. [ebook] Geneva: UNAIDS. Available at: http://data.unaids.org/pub/EPISlides/2007/2007_epiupdate_en.pdf [Accessed 3 Jun. 2014].

Underhill, K., Operario, D. and Montgomery, P. (2007). Abstinence-only programs for HIV infection prevention in high-income countries. Cochrane Database of Systematic Reviews. [online] Available at: http://dx.doi.org/10.1002/14651858.cd005421.pub2 [Accessed 3 Jun. 2014].

Vogel, M., Schwarze-Zander, C., Wasmuth, J., Spengler, U., Rockstroh, J. and Sauerbruch, T. (2010). The Treatment of Patients With HIV. DeutschesÄrzteblatt International, [online] 107(28-29), p.507. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2915483/ [Accessed 3 Jun. 2014].

Weeks, B. and Alcamo, I. (2010). AIDS. 1st ed. Sudbury, Mass.: Jones and Bartlett Publishers.

Wellensiek, B. (2007). Molecular Mechanisms of HIV-1 Infection: Viral and Host Determinants in Transmission and Pathogenesis. 1st ed. Tucson, Arizona: University of Arizona.

White, L., Duncan, G. and Baumle, W. (2011).Foundations of Adult Health Nursing. 1st ed. Clifton Park, N.Y.: Delmar/ Cengage Learning.

WHO, (2014). AntiretrovirAltherApy for hiv infection in Adults And Adolescents. 1st ed. [ebook] Geneva: WHO Press. Available at: http://whqlibdoc.who.int/publications/2010/9789241599764_eng.pdf [Accessed 3 Jun. 2014].

Winstonsmith.net, (2014). [image] Available at: http://winstonsmith.net/tumor%20transplants%20in%20human%20subjects_part2_files/image006.jpg [Accessed 3 Jun. 2014].

Wolfe, N., Switzer, W., Carr, J., Bhullar, V., Shanmugam, V., Tamoufe, U., Prosser, A., Torimiro, J., Wright, A., Mpoudi-Ngole, E., McCutchan, F., Birx, D., Folks, T., Burke, D. and Heneine, W. (2004). Naturally acquired simian retrovirus infections in central African hunters. The Lancet, [online] 363(9413), pp.932-937. Available at: http://dx.doi.org/10.1016/s0140-6736(04)15787-5 [Accessed 3 Jun. 2014].

Wright, P. (1987). “Smallpox vaccine ‘triggered Aids virus'”. The Times: London.

Paper was written & submitted by Albert Atakora

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