The human immunodeficiency virus (HIV) is a virus that progressively weakens the immune system. In the absence of treatment, it leads ultimately to the acquired immune deficiency syndrome (AIDS) and death. The purpose of this brief note is to give an overview of HIV/AIDS epidemiology: how the virus has spread and is spreading, what factors are facilitating its spread, the course of HIV infection, and interventions that can reduce the spread of HIV and alter the course of HIV infection.
Origin and spread of HIV
Many theories exist as to the possible origin of HIV. Simian immunodeficiency viruses from two primates, the sooty mangabey and the chimpanzee, have been found to be similar genetically to HIV-2 and HIV-1 respectively (Hirsch et al (1989), Huet et al (1990)). This has given strength to the most widely accepted hypothesis of origin: that HIV is the result of cross-species transfer of simian immunodeficiency viruses. Some have suggested that this transfer occurred as a result of hunting monkeys, for food or for use in laboratories, but several other theories exist (Hooper, 1999).
Although the first reported AIDS cases were among homosexuals in the United States (Gottlieb et al, 1981), earlier serological evidence of HIV suggests that HIV may have originated in the former Belgian Congo (Nahmias et al (1986), Nzilambi et al (1988)). During the 60s and 70s there was considerable migration between this country and Haiti (Piot et al, 1984), which at the time was a popular tourist destination for American homosexuals. This probably explains the high initial incidence of AIDS, observed in the United States, among homosexuals and Haitian immigrants. It was not until 1984 that it became apparent that significant heterosexual transmission of the virus was already occurring in African populations (Piot et al, 1984).
Since that time, HIV has spread to every corner of the globe, infecting individuals of all races and religions, regardless of sex or sexual orientation. It is estimated that roughly 42 million people are currently infected with HIV worldwide, and that over 20 million have died since the disease was first identified in 1981 (UNAIDS, 2002). Sub-Saharan Africa is currently the worst affected region, with roughly 29.4 million HIV infections. Numbers of infections and adult prevalence estimates for other regions are shown in Table 1 below.
HIV prevalence (%
of 15-49 age band)
South and South-East Asia
East Asia and Pacific
Eastern Europe and Central Asia
USA and Canada
North Africa and Middle East
Australia and New Zealand
Table 1: HIV infections and adult prevalence levels, by region
Source: UNAIDS (2002)
Currently, heterosexual transmission of HIV accounts for most of the HIV infection observed in Africa and the Caribbean, and is also accounting for an increasingly substantial proportion of new HIV infections in many developed countries (UNAIDS, 2002). Intravenous drug use is also a significant vector of transmission in much of Asia, Europe and North America, and has been particularly instrumental in fuelling the rapidly growing epidemics in Eastern Europe and Asia. Although there were encouraging signs that homosexual transmission was being curbed in the early stages of the AIDS epidemic, levels of homosexual transmission currently appear to be increasing in developed countries (UNAIDS, 2002). In many regions, such as North America and Latin America, all forms of transmission – heterosexual, homosexual and intravenous drug use – are common.
There are also differences between regions in terms of the strains of HIV that are common. The HIV-1 strain is most common, and is found in all parts of the world, while the HIV-2 strain is mainly confined to the countries of West Africa. HIV-2 is thought to be less infectious than HIV-1 (Kanki et al, 1994), and it has also been shown that individuals infected with HIV-2 tend to survive for longer than those infected with HIV-1 (Whittle et al, 1994). Ten subtypes of HIV-1 group M have also been identified, with substantially different geographical distributions. There is no consistent evidence, however, of differences between these subtypes in terms of their infectiousness or pathogenic potential.
Determinants of HIV prevalence
HIV prevalence levels can vary considerably between different countries and between different populations within a country. This diversity is usually attributable to a range of socio-economic, biological, demographic and behavioural factors (Johnson and Budlender, 2002).
A number of significant biological factors affect the risk of sexual transmission of HIV. The risk of HIV transmission per sexual contact is increased substantially if either partner is experiencing a sexually transmitted disease (Røttingen et al, 2001), and countries in which access to treatment for sexually transmitted diseases is poor are thus especially vulnerable to HIV. Women are also biologically more susceptible to HIV infection than men (Nicolosi et al, 1994), and the risk of HIV transmission per sexual contact is thought to be highest among younger women (Gray et al, 2001); this partly explains the high HIV prevalence levels observed in young females in purely heterosexual epidemics. It has also been shown that circumcised men are less likely to be infected with HIV than uncircumcised men (Weiss et al, 2000), and that women who use hormonal contraceptives are at a high risk of HIV infection (Wang et al (1999), Martin et al (1998)). Differences between cultures and countries in terms of contraceptive use, circumcision practices and access to treatment for sexually transmitted diseases can therefore explain much of the observed variation in HIV prevalence levels.
Related to these biological factors is the form of sex practiced. While oral sex and vaginal sex carry a relatively low risk of HIV transmission, the risk of transmission through anal intercourse is high (Leynaert et al, 1998). The high levels of HIV prevalence observed among men who have sex with men may be partially explained in terms of this, although anal intercourse is by no means an exclusively homosexual practice.
The sexual transmission of HIV is also facilitated by a range of socio-economic factors. In industrialized countries, it is usually members of ethnic minorities and poorer communities that are at greatest risk of HIV infection (UNAIDS, 2002), while in developing countries it is usually those with education and income who are at a higher risk of infection (Piot et al, 1994). In developing countries, economic migration plays an important role in the spread of the epidemic (Lurie, 2000), and accounts for the higher HIV prevalence among individuals of higher socio-economic status (particularly miners, truck drivers and security forces). The higher prevalence levels among the more affluent are also explained, to some extent, by the concentration of wealth in urban areas, where there is greater opportunity for sexual networking, and where traditional value systems have less influence on sexual behaviour. The existence of substantial income inequalities and the subordinate position of women are other factors that have fuelled the growth of the AIDS epidemic in many developing countries.
HIV prevalence levels vary considerably with age. In heterosexual epidemics, the prevalence of HIV among females is usually highest between the ages of 25 and 30, while for males prevalence usually peaks between the ages of 30 and 40 (Buvé et al, 2001). This reflects the tendency for men to seek partnerships with younger women. Below the age of 15, HIV infections are relatively rare, and usually are the result of children being infected by their HIV positive mothers, either at birth or through breastfeeding.
In addition to sexual transmission and mother-to-child transmission, the sharing of unsterilized needles by intravenous drug users is also a significant vector for HIV transmission. Studies suggest that in industrialized countries, the intravenous drug users most at risk of HIV infection are those from ethnic minorities and those with little education (Hernandez-Aguado and Bolumar (1993), Allen et al (1992)). Membership of ethnic minorities and lack of education have also been shown to be significant predictors of HIV prevalence among men who have sex with men (Catania et al (2001), Valleroy et al (2000)). The socio-economic factors driving the predominantly heterosexual epidemic in developing countries therefore differ substantially from those driving the mainly homosexual and intravenous drug user epidemics in developed countries.
The course of HIV infection
Following initial HIV infection, an individual may experience glandular fever-like symptoms that last for a few weeks. During this time, the so-called ‘window period’, an individual will test negative for HIV on antibody tests. It is only after the individual has seroconverted (i.e. started to produce antibodies to the virus), typically 3 to 4 weeks after the initial infection, that these tests will yield positive results (Lindbäck et al, 2000). Following the passing of these initial symptoms, the individual enters a prolonged asymptomatic phase, which typically lasts 4 to 6 years. The individual then starts to experience intermittently symptoms such as weight loss, diarrhoea and oral infections. Finally, when the individual’s immune system has been severely weakened by the HIV infection, they experience a variety of opportunistic infections, such as Kaposi’s sarcoma and pneumonia, which are regarded as being defining of AIDS. The term ‘AIDS’ thus refers to a range of conditions that are diagnosed in the late stages of HIV infection. In the absence of treatment, the individual typically dies within 1 to 2 years of the initial AIDS-defining illness.
The overall time from infection to death is usually estimated to be between 9 and 11 years, in the absence of treatment. It has been suggested that the median time from infection to death may be shorter in developing countries, where access to health services is poor, than in developed countries (URGEMP, 2002). However, age appears to be the most significant factor influencing the length of survival, with individuals infected at younger ages tending to survive for longer under HIV infection than those infected at older ages (CGAIHS, 2000). Although there is some evidence to suggest that genetic factors and nutritional factors may affect survival under HIV infection, there is no consistent evidence to suggest that factors such as gender, race, mode of transmission and viral subtype have any effect on survival (URGEMP, 2002).
A number of laboratory tests have been used to determine the prognosis of people infected with HIV. The two tests that are most predictive of progression to AIDS and death are the viral load test and the CD4+ lymphocyte count (Mellors et al, 1997). The CD4+ count is a measure of the degree of immune suppression; an uninfected individual would typically have a CD4+ count above 800 cells per mm3, while an individual experiencing AIDS would usually have a CD4+ count below 200. The viral load is a measure of the concentration of HIV in the body, and can be thought of as determining the rate of decline in the CD4+ count. Levels tend to be high at the time of seroconversion, and then fall gradually, rising again about two years after initial infection (Sabin et al, 1998). The viral load test is important not only as a prognostic marker, but also as a measure of an individual’s infectiousness; individuals with high viral loads are most likely to transmit HIV (Quinn et al, 2000).
Various HIV staging systems have been developed for the purposes of prognosis and setting treatment guidelines. These staging systems are based on clinical criteria (disease symptoms) and laboratory criteria (such as the CD4+ count and viral load). The Center for Disease Control use a system based on three ranges of CD4+ count (500 or greater, 200 to 499, and less than 200) and three clinical categories (asymptomatic, symptomatic with conditions attributable to HIV, and AIDS), which yields a matrix of nine disease categories (CDC, 1992). A simpler system is used by the World Health Organization; this is a four-stage system that relies only on clinical criteria (WHO, 1990).
Although individuals infected at young ages tend to survive for longer than individuals infected at older ages, children who are infected at birth are an exception. These children tend to experience relatively rapid disease progression (Taha et al, 2000), with children infected through breastmilk surviving for longer than those infected at or before birth (Spira et al, 1999). Separate staging systems tend to be used for children, as the pattern of symptoms and the prognostic values of certain markers differ between adults and children.
Prevention and treatment of HIV/AIDS
Currently there is no cure or vaccine for HIV/AIDS. However, many programmes have been developed for limiting the spread of HIV and treating HIV infection. There is much debate as to the relative cost-effectiveness of these programmes (Creese et al, 2002), and many of the assertions regarding the likely interactions between prevention and treatment initiatives are as yet unproven (Stover et al, 2002).
The most obvious technique for preventing the spread of HIV is through education and promotion of less risky sexual behaviours. This can occur through voluntary counseling and testing programmes (VCTESG, 2000), condom promotion and distribution, social marketing, mass media campaigns, peer education programmes, school-based AIDS education, and outreach programmes that target individuals at high risk of infection (Stover et al, 2002). Less obviously, programmes such as improved treatment for sexually transmitted diseases (Grosskurth et al, 1995) and needle exchange programmes (Heimer et al, 1993) have been shown to be very effective in reducing HIV transmission. The transmission of HIV from HIV positive women to their children can also be reduced through the use of antiretroviral drugs before and after birth, and through the use of formula feeding in place of breastfeeding (Dabis et al, 2000).
The treatment of HIV/AIDS is a contentious issue, with the high costs of certain forms or treatment creating an effective barrier to access in many parts of the developing world. At the most basic level, palliative care and treatment for opportunistic infections can be provided, but these have little impact on survival prospects (URGEMP, 2002). Prophylactic treatment can reduce the rate of AIDS mortality and the incidence of opportunistic infections (Badri et al, 2001), and it has also been shown that good nutrition can extend survival (Kanter et al, 1999). However, the most significant form of treatment, in terms of reducing mortality and morbidity, is antiretroviral therapy. Initially, single-drug therapy and dual therapy yielded modest reductions in rates of morbidity and mortality, but more dramatic reductions have been achieved since the development of new classes of antiretroviral drugs in the mid-1990s (Jordan et al, 2002). The terms ‘highly active antiretroviral therapy’ (HAART) and ‘triple therapy’ typically refer to the use of these new drugs in combination with the earlier dual therapy regimens.
While the above prevention and treatment programmes are crucial in alleviating the impact of HIV/AIDS at an individual level, it is also important that interventions be developed with a view to the social determinants of HIV risk, and the social impacts of the AIDS epidemic. As discussed previously, factors such as gender inequality, migration and stigma around AIDS fuel the growth of the epidemic, and these need to be addressed. Similarly, policy makers need to look beyond caring for those dying of AIDS, and need to consider orphan care programmes in severely affected communities.
Allen D., Onorato I. and Green T. (1992) HIV infection in intravenous drug users entering drug treatment, United States, 1988 to 1989. American Journal of Public Health. Vol. 82(4), 541 – 546
Badri M., Ehrlich R., Wood R. and Maartens G. (2001) Initiating co-trimoxazole prophylaxis in HIV-infected patients in Africa: an evaluation of the provisional WHO/UNAIDS recommendations. AIDS. Vol. 15, 1143 – 1148
Buvé A., Caraël M., Hayes R. et al. (2001) Multicentre study on factors determining differences in rate of spread of HIV in sub-Saharan Africa: methods and general population prevalence of HIV. AIDS. Vol. 15 (suppl 4), S5 – S14
Catania J., Osmond D., Stall R. et al. (2001) The continuing epidemic among men who have sex with men. American Journal of Public Health. Vol. 91(6), 907 – 914
Center for Disease Control (CDC). (1992) 1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. Morbidity and Mortality Weekly Report. Vol. 41(RR-17), December 18. Available: www.cdc.gov/mmwr/preview/mmwrhtml/00018871.htm. Accessed November 2002
Collaborative Group on AIDS Incubation and HIV Survival (CGAIHS). (2000) Time from HIV-1 seroconversion to AIDS and death before widespread use of highly-active antiretroviral therapy: a collaborative re-analysis. The Lancet. Vol. 355, 1131 – 1137
Creese A., Floyd K., Alban A. and Guiness L. (2002) Cost-effectiveness of HIV/AIDS interventions in Africa: a systematic review of the evidence. The Lancet. Vol. 359, 1635 – 1642
Dabis F., Leroy V., Castetbon K. et al. (2000) Preventing mother-to-child transmission of HIV-1 in Africa in the year 2000. AIDS. Vol. 14, 1017 – 1026
Gottlieb M., Schanker H., Saxon A. et al. (1981) Pneumocystis pneumonia – Los Angeles. Morbidity and Mortality Weekly Report. Vol.30, 250 – 252
Gray R., Wawer M., Brookmeyer R. et al. (2001) Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda. The Lancet. Vol. 357, 1149 – 1153
Grosskurth H., Hosha F., Todd J. et al. (1995) Impact of improved treatment of sexually transmitted diseases on HIV infection in rural Tanzania: randomised control trial. The Lancet. Vol. 346, 530 – 536
Heimer R., Kaplan E., Koshnood K. et al. (1993) Needle exchange decreases the prevalence of HIV-1 proviral DNA in returned syringes in New Haven, Connecticut. American Journal of Medine. Vol. 95, 214 – 220
Hernandez-Aguado I. and Bolumar F. (1993) Determinants of HIV-1 infection in intravenous drug users in Valencia, Spain, 1987 – 1991. International Journal of Epidemiology. Vol. 22(3), 537 – 542
Hirsch V., Olmsted R, Murphy-Corb M. et al. (1989) An African primate lentivirus (SIVsm) closely related to HIV-2. Nature. 1989. Vol. 339, 389 – 392
Hooper E. (1999) The River: a journey back to the source of HIV and AIDS. Penguin Books. London
Huet T., Cheynier R., Meyerhans A. et al. (1990) Genetic organization of a chimpanzee lentivirus related to HIV-1. Nature. Vol. 345, 356 – 359
Johnson L. and Budlender D. (2002) HIV risk factors: a review of the demographic, socio-economic, bio-medical and behavioural determinants of HIV prevalence in South Africa. CARE Monograph No. 8. Centre for Actuarial Research, University of Cape Town. Available:
Jordan R., Gold L., Cummins C. and Hyde C. (2002) Systematic review and meta-analysis of evidence for increasing numbers of drugs in antiretroviral combination therapy. British Medical Journal. Vol. 324, 1 – 10
Kanki P., Travers K., Mboup S. et al. (1994) Slower heterosexual spread of HIV-2 than HIV-1. The Lancet. Vol. 343, 943 – 946
Kanter A., Spencer D., Steinberg M. et al. (1999) Supplemental vitamin B and progression to AIDS and death in black South Africans infected with HIV. Journal of Acquired Immune Deficiency Syndrome. Vol. 21, 252
Leynaert B., Downs A., and de Vincenzi I. (1998) Heterosexual transmission of Human Immunodeficiency Virus: variability of infectivity throughout the course of infection. American Journal of Epidemiology. Vol. 148(1), 88 – 96
Lindbäck S., Thorstensson R., Karlsson A. et al. (2000) Diagnosis of primary HIV-1 infection and duration of follow-up after HIV exposure. AIDS. Vol. 14, 2333 – 2339
Lurie M. (2000) Migration and AIDS in southern Africa: a review. South African Journal of Science. Vol. 96, 343 – 347
Martin H., Nyange P., Richardson B. et al. (1998) Hormonal contraception, sexually transmitted diseases, and the risk of heterosexual transmission of human immunodeficiency virus type 1. Journal of Infectious Diseases. Vol. 178, 1053 – 1059
Mellors J., Muñoz A., Giorgi J. et al. (1997) Plasma viral load and CD4+ lymphocytes as prognostic markers of HIV-1 infection. Annals of Internal Medicine. Vol. 126, 946 – 954
Nahmias A., Weiss J., Yao X. et al. (1986) Evidence for human infection with an HTLV III/LAV-like virus in Central Africa, 1959. The Lancet. Vol. 1(ii), 1279 – 1280
Nicolosi A., Leite M., Musicco M. et al. (1994) The efficiency of male-to-female and female-to-male sexual tranmission of the Human Immunodeficiency Virus: a study of 730 stable couples. Epidemiology. Vol. 5(6), 570 – 575
Nzilambi N., De Cock K., Forthal D. et al. (1988) The prevalence of infection with human immunodeficiency virus over a 10-year period in rural Zaire. New England Journal of Medicine. Vol. 318, 276 – 279
Piot P., Goeman J and Laga M. (1994) The epidemiology of HIV and AIDS in Africa (Chapter 13). In Essex M., Mboup S., Kanki P. and Kalengayi M. (editors). AIDS in Africa. Raven Press. New York
Piot P., Taelman H., Minlangu K. et al. (1984) Acquired immune deficiency syndrome in a heterosexual population in Zaire. The Lancet. Vol. 2, 65 – 69
Quinn T., Wawer M., Sewankambo N. et al. (2000) Viral load and heterosexual transmission of human immunodeficiency virus type 1. New England Journal of Medicine. Vol. 342, 921 – 929
Røttingen J., Cameron D. and Garnett G. (2001) A systematic review of the epidemiological interactions between classic sexually transmitted diseases and HIV: how much is really known? Sexually Transmitted Diseases. Vol. 28(10), 579 – 597
Sabin C., Mocroft A., Cozzi Lepri A. and Philips A. (1998) Cofactors and markers of disease progression in human immunodeficiency virus infection. Journal of the Royal Statistical Society, Series A. Vol. 161(2), 177 – 189
Spira R., Lepage P., Msellati P. et al. (1999) Natural History of Human Immunodeficiency Virus Type 1 Infection in Children: A Five-Year Prospective Study in Rwanda. Pediatrics Vol. 104, No. 5
Stover J., Walker N., Garnett G. et al. (2002) Can we reverse the HIV/AIDS pandemic with an expanded response? The Lancet. Vol. 360, 73 – 77
Taha T., Graham S., Kumwenda N. et al. (2000) Morbidity among human immunodeficiency vius-1-infected and –uninfected African children. Pediatrics. Vol. 106, No.6
UNAIDS Reference Group on Estimates, Modelling and Projections (URGEMP). (2002) Improved methods and assumptions for estimation of the HIV/AIDS epidemic and its impact: recommendations of the UNAIDS Reference Group on Estimates, Modelling and Projections. AIDS. Vol. 16, WHO-UNAIDS Report, W1 – W14
Valleroy L., MacKellar D., Karon J. et al. (2000) HIV prevalence and associated risks in young men who have sex with men. Journal of the American Medical Association. Vol. 284(2), 198 – 204
Voluntary HIV-1 Counselling and Testing Efficacy Study Group (VCTESG). (2000) Efficacy of voluntary HIV-1 counselling and testing in individuals and couples in Kenya, Tanzania and Trinidad: a randomised trial. The Lancet. Vol. 356, 103 – 112
Wang C., Reilly M. and Kreiss J. (1999) Risk of HIV infection in oral contraceptive pill users: a meta-analysis. Journal of Acquired Immune Deficiency Syndrome. Vol. 21(1), 51 – 58
Weiss H., Quigley M. and Hayes R. (2000) Male circumcision and risk of HIV infection in sub-Saharan Africa: a systematic review and meta-analysis. AIDS. Vol. 14, 2361 – 2370
Whittle H., Morris J., Todd J. et al. (1994) HIV-2-infected patients survive longer than HIV-1-infected patients. AIDS. Vol. 8, 1617 – 1620
World Health Organization (WHO). (1990) Acquired Immunodeficiency Syndrome (AIDS). Interim proposal for a WHO staging system for HIV infection and disease. Weekly Epidemiological Record. Vol. 65, 221 – 224