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Chapter 1:   What is HIV?
Chapter 2:   Classification of HIV
Chapter 3:   Where does HIV come from?
Chapter 4:   How is HIV spread?
Chapter 5:   How do you diagnose HIV?
Chapter 6:   Natural history of HIV?
Chapter 7:   How common is HIV?
Chapter 8:   What is AIDS?
Chapter 9:   Is there a cure for AIDS?
Chapter 10: How do you treat AIDS?
Chapter 11: How has AIDS affected S.A?
Chapter 12: How do you prevent HIV?
Chapter 13: HIV prevention strategies under development.


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Acquired Immunodeficiency Syndrome (AIDS) is the world’s most devastating epidemic in the history of humankind. Since the first reported cases of AIDS in 1981, more than 70 million people have been infected with the Human Immunodeficiency Virus (HIV). HIV is a retrovirus that causes AIDS and is spread from mother-to-child, through blood contamination and through sex. When spread, HIV specifically enters, infects and grows in the human body’s cells that have a CD4 receptor. After HIV multiplies in a CD4+ cell, it dies - releasing hundreds of new HIV into the body. This process leads to the systematic destruction and loss of CD4+ cells over a period of years. During this period, which is on average about 7 years, the person is asymptomatic with HIV infection, but is infectious, thereby creating the conditions for the efficient spread of this virus. After a period ranging from a year to many years, the CD4+ cell numbers drop to low levels and the person is then unable to develop a proper immune response, ie. immune deficiency. This immunodeficiency state makes the person susceptible to various opportunistic infections and malignancies, which signal the onset of AIDS. In this short book, we describe HIV, how it is classified and where it originated from. We also provide an overview of the extent of the epidemic, how HIV is spread, how it can be diagnosed and briefly describe the spectrum of opportunistic diseases and malignancies associated with AIDS. The significant scale up of antiretroviral therapy over the past decade in sub-Saharan Africa has transformed perceptions of AIDS from a plague to a manageable, chronic illness. The emerging challenges of drug resistance are discussed in the context of an ever expanding treatment programme. A section is dedicated to the impact of HIV and AIDS on South Africans. Specifically, the impact of AIDS on the health care burden, the impact on society, the economic impact of AIDS and the impact of mortality are discussed. Significant progress has been made in the prevention of mother-to-child transmission and prevention of sexual transmission. Each of the proven HIV prevention methods, including: sexual abstinence, monogamy, condoms, treatment of concurrent sexually transmitted infections, prophylactic treatment with antiretrovirals, male circumcision and HIV counselling and testing are discussed. The progress and challenges of developing a successful HIV vaccine are also discussed. The advances in HIV treatment and recent advances in the use of antiretrovirals for HIV prevention have created a newfound optimism that it may be possible to control the HIV epidemic.

2015-12-15 04-11-07 PM

Dr Aaron Motsoaledi MBChB Minister of Health South Africa

2015-12-15 04-10-33 PM

Professor Salim S. Abdool Karim MBChB, PhD Director: CAPRISA President, Medical Research Council of South Africa. Pro Vice-Chancellor (Research),University of KwaZulu-Natal. Professor of Clinical Epidemiology,Columbia University. Adjunct Professor of Medicine, Cornell University Associate Member, The Ragon Institute of MGH, MIT and Harvard University

Chapter 5


The first commercially available HIV serological tests were available by 1985. Subsequently there has been a rapid evolution in HIV diagnostic technology. Currently, a wide range of assays are available for adult and pediatric diagnosis, monitoring disease progression and therapeutic success, as well as for research and surveillance. These assays can be performed on a range of biological tissues such as serum, plasma, saliva, whole blood, urine, seminal fluid and cervico-vaginal specimens. 2015-12-15 09-41-05 AM FIGURE 6 : Raid HIV antibody test showing a positive (left) and negative (right) result

ANTIBODY DETECTION Detection of antibodies using serological tests such as a standard enzyme immunoassay (EIA) is most often used for screening or diagnosis of HIV infection. A major advance has been the availability of rapid HIV antibody tests (Figure 6) and results are available within minutes. The two limitations of these serological tests are, firstly, detection of infection during primary infection when antibody levels are low or absent and secondly, determination of whether a reactive EIA or positive rapid HIV test in newborns is due to infection in the baby or due to passively transferred maternal antibodies. In these instances, the use of polymerase chain reaction (PCR) technology for detection of viral RNA is helpful. ANTIGEN DETECTION Standard EIA tests are available for detecting p24 antigen, which is often the earliest antigen that can be detected in acute HIV infection before the presence of antibodies is detectable. It is therefore used to identify the presence of HIV infection during the window period, the period between onset of HIV infection and the detection of HIV antibodies. NUCLEIC ACID DETECTION Plasma viral load is a marker of viral replication and is used to monitor therapeutic success in patients on antiretroviral treatment. A number of commercially available tests provide sensitive quantification as low as 50 copies of HIV RNA copies per ml. There are also tests for cell-associated HIV which measure branched DNA levels. CD4+ CELL COUNTS The number of CD4+ T-cells reveals the degree of immunodeficiency and is therefore a key criterion for initiating antiretroviral treatment. At present, flow cytometry analysis is the standard method for quantification of CD4+ cells. Where CD4+ quantification is not readily available, total white cell counts are sometimes used as a proxy marker. T-CELL IMMUNE RESPONSE DETECTION Various assays have been developed to assess the presence of a cellular immune response to HIV antigens. The earlier approaches like the Chromium release assay and the tetramer assay have now largely been superseded by the Elispot assay and the Intracellular cytokine stain assay. The latter two assays depend on the release of certain cytokines, such an interferon-gamma, when T-cells from the patient recognize HIV antigens used in the test. These assays are very sensitive and can sometimes be positive in the absence of any other markers of HIV infection – suggesting that the patient has previously encountered and can recognize HIV antigens, perhaps through a previous HIV exposure or aborted HIV infection. The hypotheses of aborted HIV infection and clearance of established HIV infection have not been confirmed empirically. ASSAYS TO IDENTIFY RECENT HIV INFECTION For research and surveillance purposes, differentiating between established/prevalent infection and new/incident HIV infections is critical for monitoring trends in the epidemic or efficacy of new interventions under trial. A number of tests have been developed for this purpose; most are based on differences between antibody responses in early versus established HIV infection. The three most commonly used serologic assays for estimating incidence from prevalent studies are the “detuned” or STARHS (Serologic Testing Algorithm for Recent HIV Seroconversion) assay, Immunoglobulin G (IgG) Capture BED-enzyme immunoassay (BED-CEIA) and the Avidity Index (AI). All of these assays have substantial limitations and tend to over-estimate the incidence of infection due to their high false positive rates. STARHS consists of a less sensitive, first-generation ELISA followed by a later-generation ELISA with increased sensitivity. Recent infection (within the last 129 days, depending on viral sub-type) is indicated if the first-generation ELISA is negative and the second-generation ELISA is positive. The BED-CEIA attempts to identify recent HIV infection by measuring increasing levels of anti-IgG as a proportion of overall IgG. Recent infection (within the last 153 days) is indicated by a ratio of HIV-specific IgG/total IgG less than 0.8.

Other assays in development are the Affinity assay, IgG3 isotype assay and anti-HIV p31 assay.