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.