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Chapter 2 Literature review on Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS)
General
HIV is a disease that is feared all over the world. It was already discovered in 1981, and 24 years later this disease has reached devastating effects with millions affected all over the world. The disease was first recognised when small clusters of young homosexual men in American cities were reported to suffer rare opportunistic infections like Pneumocystis carnii and Kaposi’s sarcoma (Hochauser & Rothenberger, 1992). Initially it was not sure if the disease was a « gay disease » and if it was spread by other means as well. By early 1982 reports of Acquired Immune Deficiency Syndrome (AIDS) in recipients of blood transfusions and pooled clotting factors, as well as among injecting drug users indicated that an infectious agent was to blame. The appearance in Africa and in Haiti suggested that the unknown pathogen was already widespread in countries all over the world (Mims et al., 1999). In 1983 Francoise Barré-Sinoussi and colleagues isolated their first virus from a patient at the Institut Pasteur in France. The patient had persistent lymphadenopathy and the virus was named the lymphadenopathy-associated virus. By April 1984 the French group had already isolated two more, one from an AIDS patient. A month later Gallo’s group at the US National Institutes of Health (NIH) reported retroviruses that they named human T-lymphotropic virus type III or HTLV-III (Gallo et al., 1984). Levy et al., 1984 also independently isolated AIDS-related retroviruses. The term Human Immunodeficiency Virus (HIV) was adopted in 1986 (Smith et al., 2001).By 1986 the drug zidovudine (AZT) had become available, though its effectiveness was still to be measured. As the decade of the 1980’s advanced, it became clear that the effects of HIV infection were variable and not necessarily confined to the lifethreatening conditions identified in the official definitions of AIDS (Anderson &Wilkie, 1992). HIV positive refers to a condition where the person is infected with the virus. This does not necessarily mean that the patient will show symptoms, or will feel any different than a HIV negative person. It is only until the disease progresses to AIDS when the person starts to show symptoms and it is often recognised by the development of HIV-related diseases such as pneumonia and tuberculosis. Several stages in the development of an HIV infection to the condition of AIDS have been identified (Figure 2.1). After infection with the virus, the person will enter the window period, with no signs or symptoms indicating infection. The virus will infect mostly CD4 cells. CD4 receptor sites on helper T-cells serves as a marker to distinguish them from other T-cells. That is the reason for these cells to be named CD4 cells or T4 cells. After infection the body’s immune system will produce antibodies against the foreign virus particles called antigens. It takes six to eight weeks for these antibodies to be produced. The virus can not be detected during the window period, because conventional HIV tests test for the antibodies produced against the virus, which is not present in high enough quantities during the first six to eight weeks. People are therefore advised to repeat the test after eight weeks to eliminate the window period, and detect the antibodies that would have been formed after eight weeks or longer After the window period a short acute period follows with very mild symptoms like flu, fever and swollen lymph glands, which could last for a day or two. The symptoms are so mild and common that few people would recognise these symptoms as warnings signs of HIV infection. People with HIV may remain healthy and show no symptoms for many years during the asymptomatic phase. This phase varies between individuals, depending on the strength of the body and the immune system, and might only last for a few months or could continue for many years. This phase has been monitored in individuals for twenty years or even more. Later in the course of infection, harmful changes to the immune system may be observed, and the development of HIV-related problems might occur. These people can also develop opportunistic infections (OI) and cancers that can be life threatening.
Chapter 1: Introduction & Background
1.1 General introduction
1.2 Background on traditional medicine
1.3 Objectives and hypothesis
1.4 Plant selection
1.5 The genus Elaeodendron Jacq
1.6 Elaeodendron croceum (Thunb) DC
1.7 Compounds previously isolated from E. croceum
1.8 Compounds previously isolated from Elaeodendron spp.
1.8.1 E. buchananii
1.8.2 E. glaucum
1.8.3 E. transvaalensis
1.8.4 E. balae
1.9 Discussion
Chapter 2: Literature review on Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS)
2.1 General
2.2 Structure of a virus
2.3 Pathogenesis
2.4 Current anti-retroviral drugs and their mode of action
2.5 The immune system
2.5.1Antigens
2.5.2 Antibodies
2.5.3 T-cell receptors
2.5.4 Cytokines
2.5.5 The effect of HIV on the immune system
2.5.6 Antibody tests
2.5.7 HIV antigen tests
2.5.8 Monitoring the effects of HIV
2.6 HIV/AIDS Statistics
2.6.1 Sub-Saharan Africa
2.6.2 South Africa
Chapter 3: Extract preparation, isolation and identification of active compounds from Elaeodendron croceum
3.1 Introduction
3.2 Materials and methods
3.2.1 Plant selection
3.2.2 Extract preparation
3.2.3 Isolation of active compounds
3.2.4 Identification of the active compounds
3.3 Results
3.4 Discussion
Chapter 4: Anti-HIV activity of Elaeodendron croceum extract and isolated compound
4.1 Introduction
4.2 Materials and methods
4.2.1Materials
4.2.2 Reverse Transcriptase
4.2.3 NF-κB and Tat
4.2.4 HeLa-Tat-Luc
4.2.5 VSV Pseudotype
4.3 Results
4.4 Discussion
Chapter 5: Toxicity of Elaeodendron croceum extract and isolated compound
5.1 Introduction
5.2 Materials and methods
5.2.1 Preparation of Minimal Essential Medium (MEM)
5.2.2 Preparation of cells for toxicity screen
5.2.3 Preparation of crude extract and pure compounds
5.3 Results
5.4 Discussion
Chapter 6: Review on digitoxigenin-glucoside and related cardiac glycosides
6.1 Introduction
6.2 Digitoxigenin-3-O-glucoside
6.3 Related cardiac glycosides
6.3.1 3,14-Dihydroxycard-20(22)-enolide
6.3.2 Digoxin
6.3.3 Digitoxin
6.3.4 Actodigin
6.3.5 Glycyrrhizic acid
6.4 Discussion
Chapter 7: General discussion and conclusion
Chapter 8: Acknowledgements
Chapter 9: Summary
Chapter 10: References
