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HIV-AIDS - A Very Short Introduction
HIV-AIDS - A Very Short Introduction
Alan Whiteside
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HIV/AIDS is without doubt the worst epidemic to hit humankind since the Black Death. As of 2004 an estimated 40 million people were living with the disease, and about 20 million had died. Despite rapid scientific advances there is still no cure and the drugs are expensive and toxic. In the developing world, especially in parts of Africa, life expectancy has plummeted to below 35 years, causing a serious decline in economic growth, a sharp increase in orphans, and the imminent collapse of health care systems. The news is not all bleak though. There have been unprecedented breakthroughs in understanding diseases and developing drugs. Because the disease is so closely linked to sexual activity and drug use, the need to understand and change behavior has caused us to reassess what it means to be human and how we should operate in the globalizing world. This Very Short Introduction tackles the science, the international and local politics, the fascinating demographics, and the devastating consequences of the disease, and suggests how we must respond.
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Oxford University Press, USA
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Very Short Introductions
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HIV/AIDS: A Very Short Introduction VERY SHORT INTRODUCTIONS are for anyone wanting a stimulating and accessible way in to a new subject. They are written by experts, and have been published in more than 25 languages worldwide. The series began in 1995, and now represents a wide variety of topics in history, philosophy, religion, science, and the humanities. Over the next few years it will grow to a library of around 200 volumes – a Very Short Introduction to everything from ancient Egypt and Indian philosophy to conceptual art and cosmology. Very Short Introductions available now: AFRICAN HISTORY John Parker and Richard Rathbone AMERICAN POLITICAL PARTIES AND ELECTIONS L. Sandy Maisel THE AMERICAN PRESIDENCY Charles O. Jones ANARCHISM Colin Ward ANCIENT EGYPT Ian Shaw ANCIENT PHILOSOPHY Julia Annas ANCIENT WARFARE Harry Sidebottom ANGLICANISM Mark Chapman THE ANGLO-SAXON AGE John Blair ANIMAL RIGHTS David DeGrazia ANTISEMITISM Steven Beller ARCHAEOLOGY Paul Bahn ARCHITECTURE Andrew Ballantyne ARISTOTLE Jonathan Barnes ART HISTORY Dana Arnold ART THEORY Cynthia Freeland THE HISTORY OF ASTRONOMY Michael Hoskin ATHEISM Julian Baggini AUGUSTINE Henry Chadwick BARTHES Jonathan Culler BESTSELLERS John Sutherland THE BIBLE John Riches THE BRAIN Michael O’Shea BRITISH POLITICS Anthony Wright BUDDHA Michael Carrithers BUDDHISM Damien Keown BUDDHIST ETHICS Damien Keown CAPITALISM James Fulcher THE CELTS Barry Cunliffe CHAOS Leonard Smith CHOICE THEORY Michael Allingham CHRISTIAN ART Beth Williamson CHRISTIANITY Linda Woodhead CLASSICS Mary Beard and John Henderson CLASSICAL MYTHOLOGY Helen Morales CLAUSEWITZ Michael Howard THE COLD WAR Robert McMahon CONSCIOUSNESS Susan Blackmore CONTEMPORARY ART Julian Stallabrass CONTINENTAL PHILOSOPHY Simon Critchley COSMOLOGY Peter Coles THE CRUSADES Christopher Tyerman CRYPTOGRAPHY Fred Piper and Sean Murphy DADA AND SURREALISM David Hopkins DARWIN Jonathan Howard THE DEAD SEA SCROLLS Timothy Lim DEMOCRACY Bernard Crick DESCARTES Tom Sorell DESIGN John; Heskett DINOSAURS David Norman DOCUMENTARY FILM Patricia Aufderheide DREAMING J. Allan Hobson DRUGS Leslie Iversen THE EARTH Martin Redfern ECONOMICS Partha Dasgupta EGYPTIAN MYTH Geraldine Pinch EIGHTEENTH-CENTURY BRITAIN Paul Langford THE ELEMENTS Philip Ball EMOTION Dylan Evans EMPIRE Stephen Howe ENGELS Terrell Carver ETHICS Simon Blackburn THE EUROPEAN UNION John Pinder and Simon Usherwood EVOLUTION Brian and Deborah Charlesworth EXISTENTIALISM Thomas Flynn FASCISM Kevin Passmore FEMINISM Margaret Walters THE FIRST WORLD WAR Michael Howard FOSSILS Keith Thomson FOUCAULT Gary Gutting THE FRENCH REVOLUTION William Doyle FREE WILL Thomas Pink FREUD Anthony Storr FUNDAMENTALISM Malise Ruthven GALILEO Stillman Drake GAME THEORY Ken Binmore GANDHI Bhikhu Parekh GEOPOLITICS Klaus Dodds GLOBAL CATASTROPHES Bill McGuire GLOBALIZATION Manfred Steger GLOBAL WARMING Mark Maslin THE GREAT DEPRESSION AND THE NEW DEAL Eric Rauchway HABERMAS James Gordon Finlayson HEGEL Peter Singer HEIDEGGER Michael Inwood HIEROGLYPHS Penelope Wilson HINDUISM Kim Knott HISTORY John H. Arnold HIV/AIDS Alan Whiteside HOBBES Richard Tuck HUMAN EVOLUTION Bernard Wood HUMAN RIGHTS Andrew Clapham HUME A. J. Ayer IDEOLOGY Michael Freeden INDIAN PHILOSOPHY Sue Hamilton INTELLIGENCE Ian J. Deary INTERNATIONAL MIGRATION Khalid Koser INTERNATIONAL RELATIONS Paul Wilkinson ISLAM Malise Ruthven JOURNALISM Ian Hargreaves JUDAISM Norman Solomon JUNG Anthony Stevens KABBALAH Joseph Dan KAFKA Ritchie Robertson KANT Roger Scruton KIERKEGAARD Patrick Gardiner THE KORAN Michael Cook LINGUISTICS Peter Matthews LITERARY THEORY Jonathan Culler LOCKE John Dunn LOGIC Graham Priest MACHIAVELLI Quentin Skinner THE MARQUIS DE SADE John Phillips MARX Peter Singer MATHEMATICS Timothy Gowers MEDICAL ETHICS Tony Hope MEDIEVAL BRITAIN John Gillingham and Ralph A. Griffiths MODERN ART David Cottington MODERN IRELAND Senia Pašeta MOLECULES Philip Ball MUSIC Nicholas Cook MYTH Robert A. Segal NATIONALISM Steven Grosby THE NEW TESTAMENT AS LITERATURE Kyle Keefer NEWTON Robert Iliffe NIETZSCHE Michael Tanner NINETEENTH-CENTURY BRITAIN Christopher Harvie and H. C. G. Matthew NORTHERN IRELAND Marc Mulholland PARTICLE PHYSICS Frank Close PAUL E. P. Sanders PHILOSOPHY Edward Craig PHILOSOPHY OF LAW Raymond Wacks PHILOSOPHY OF SCIENCE Samir Okasha PHOTOGRAPHY Steve Edwards PLATO Julia Annas POLITICS Kenneth Minogue POLITICAL PHILOSOPHY David Miller POSTCOLONIALISM Robert Young POSTMODERNISM Christopher Butler POSTSTRUCTURALISM Catherine Belsey PREHISTORY Chris Gosden PRESOCRATIC PHILOSOPHY Catherine Osborne PSYCHOLOGY Gillian Butler and Freda McManus PSYCHIATRY Tom Burns QUANTUM THEORY John Polkinghorne RACISM Ali Rattansi THE RENAISSANCE Jerry Brotton RENAISSANCE ART Geraldine A. Johnson ROMAN BRITAIN Peter Salway THE ROMAN EMPIRE Christopher Kelly ROUSSEAU Robert Wokler RUSSELL A. C. Grayling RUSSIAN LITERATURE Catriona Kelly THE RUSSIAN REVOLUTION S. A. Smith SCHIZOPHRENIA Chris Frith and Eve Johnstone SCHOPENHAUER Christopher Janaway SHAKESPEARE Germaine Greer SIKHISM Eleanor Nesbitt SOCIAL AND CULTURAL ANTHROPOLOGY John Monaghan and Peter Just SOCIALISM Michael Newman SOCIOLOGY Steve Bruce SOCRATES C. C. W. Taylor THE SPANISH CIVIL WAR Helen Graham SPINOZA Roger Scruton STUART BRITAIN John Morrill TERRORISM Charles Townshend THEOLOGY David F. Ford THE HISTORY OF TIME Leofranc Holford-Strevens TRAGEDY Adrian Poole THE TUDORS John Guy TWENTIETH-CENTURY BRITAIN Kenneth O. Morgan THE VIKINGS Julian Richards WITTGENSTEIN A. C. Grayling WORLD MUSIC Philip Bohlman THE WORLD TRADE ORGANIZATION Amrita Narlikar Available soon: 1066 George Garnett EXPRESSIONISM MODERN CHINA Rana Mitter NELSON MANDELA Katerina Reed-Tsocha GALAXIES John Gribbin GEOGRAPHY John Matthews and David Herbert GERMAN LITERATURE Nicholas Boyle Elleke Boehmer NUCLEAR WEAPONS Joseph M. Siracusa QUAKERISM Pink Dandelion SCIENCE AND RELIGION Thomas Dixon HISTORY OF MEDICINE William Bynum MEMORY Jonathan Foster SEXUALITY Véronique Mottier THE MEANING OF LIFE Terry Eagleton For more information visit our website www.oup.co.uk/general/vsi/ Alan Whiteside HIV/AIDS A Very Short Introduction 1 1 Great Clarendon Street, Oxford OX2 6DP Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide in Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With offices in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Thailand Turkey Ukraine Vietnam Oxford is a registered trade mark of Oxford University Press in the UK and in certain other countries Published in the United States by Oxford University Press Inc., New York Alan Whiteside 2008 The moral rights of the author have been asserted Database right Oxford University Press (maker) First published as a Very Short Introduction 2008 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above You must not circulate this book in any other binding or cover and you must impose the same condition on any acquirer British Library Cataloguing in Publication Data Data available Library of Congress Cataloging in Publication Data Data available ISBN 978–0–19–280692–5 1 3 5 7 9 10 8 6 4 2 Typeset by SPI Publisher Services, Pondicherry, India Printed in Great Britain by Ashford Colour Press Ltd, Gosport, Hampshire Contents Preface xi Abbreviations xv List of illustrations xvii List of tables xix 1 2 3 4 5 6 7 8 The emergence and state of the HIV/AIDS epidemic 1 How HIV/AIDS works and scientific responses 22 The factors that shape different epidemics 39 Illness, deaths, and populations 55 The impact of AIDS on production and people 67 AIDS and politics 85 Responding to HIV/AIDS 103 The next 25 years 123 References and further reading 133 Index 142 This page intentionally left blank Preface It is over a quarter of a century since clinicians in the USA identified the first cases of the syndrome that came to be known as AIDS. These reports simply referred to groups of people with unusual illnesses. Today AIDS is the major killer of young adults, globally 40 million people are infected, the vast majority in developing countries, and numbers continue to rise. I first took notice of HIV/AIDS in 1987 when researching labour migration in Southern Africa. Apartheid and the legacy of colonialism created the perfect hothouse for the spread of a sexually transmitted disease. What started as an academic and intellectual exercise became intensely personal. The HIV prevalence in Swaziland, where I grew up, rose from 3.9% among pregnant women in 1992, to 42.6% in the 2004 survey. I live in South Africa, where AIDS affects us all as we watch colleagues, friends, neighbours, and co-workers fall ill and die. We converse about and take these deaths in our stride in a way that is abnormal but unremarked. We have made huge progress in understanding the science of the retrovirus that causes AIDS: where it came from, how it works, and how it spreads; we are still a long way from having a cure or vaccine and have proven lamentably inadequate at stopping its progress in many communities. Medical advances mean that there are treatments available that can prolong life, although they are expensive and complex and do not cure. This Very Short Introduction is about a unique and dynamic disease that has long-term consequences. It provides an introduction to the science around the pandemic but focuses on the profound impacts AIDS is having on households, communities, and on national demographic and development indicators. We are seeing adults dying, orphans left behind, women unevenly burdened by care, impacts on civil society groups, on politicians, and a general atmosphere of ‘dis-ease’. In order to understand the effects of AIDS, we need to extend the time frame, to take a longer-term perspective: macro impacts take decades to unfold. This disease is a long-wave event, and we must look into the future to understand and respond to its consequences. The burden of HIV/AIDS is not borne equally. It is the deprived and powerless who are most likely to be infected and affected. AIDS is primarily a disease of the poor, be they poor nations or poor people in rich nations. Geographically the worst epidemics are in sub-Saharan Africa, specifically Southern Africa, and many examples in this introduction are drawn from here. HIV/AIDS is a global phenomenon but the dynamics and its consequences are played out differently across the world. This introduction looks at the epidemics and what they mean for countries, populations, production, and reproduction. It reflects that AIDS calls on us to assess what is important to us and how we relate to each other, in our communities but also globally. It asks if it matters if a young Swazi girl has a greater than 80% chance of dying from AIDS in her lifetime. What does it mean for older women caring for their children’s children? The answers are not clear or simple. There are unexpected signs of hope. In particular, there is a coming together in South African society that is reminiscent of the fight against apartheid. Will this mobilization and unity so essential to stopping the disease be repeated elsewhere? Writing a short book proved more difficult than I would ever have believed. I would like to express my appreciation to many people for their help and support: the OUP staff, in particular Luciana O’Flaherty, who read and commented on numerous drafts, Marsha Filion, and James Thompson; in Durban, the Health Economics and HIV/AIDS Research Division staff; my family Ailsa Marcham, Rowan Whiteside, and Douglas Whiteside; and friends, colleagues, and readers, specifically Tony Barnett, May Chazan, Stephanie Nixon, Nana Poku, Judith Shier, Tim Quinlan, Obed Qulo, Jon Simon, and Alex de Waal, and the OUP readers. This page intentionally left blank Abbreviations AIDS ANC ART AZT CBR CDR CDC CIHD DFID DNA DHS ELISA GDP GPA HDI HIV IDU MDG MDR TB MTCT NGO PEPFAR RNA SARS SIDA SIV SSA STI acquired immunodeficiency syndrome antenatal clinic antiretroviral therapies azidothymidine crude birth rate crude death rate Centers for Disease Control Center for International Health and Development Department for International Development deoxyribonucleic acid demographic health survey enzyme-linked immunosorbent assay gross domestic product Global Programme on AIDS Human Development Index human immunodeficiency virus intravenous drug user Millennium Development Goal multi-drug-resistant tuberculosis mother-to-child transmission non-governmental organization Presidential Emergency Plan for AIDS Relief ribonucleic acid severe acute respiratory syndrome syndrome d’immunodéficience acquise simian immunodeficiency viruses sub-Saharan Africa sexually transmitted infection TAC TB TFR UNAIDS UNDP UNFPA UNICEF USAID WHO XDR TB Treatment Action Campaign tuberculosis total fertility rate Joint United Nations Programme on HIV/AIDS United Nations Development Programme United Nations Fund for Population Activities United Nations Children’s Fund United States Agency for International Development World Health Organization extensively drug-resistant tuberculosis List of illustrations 1 Epidemic curves 5 2 Southern African epidemics: HIV prevalence in antenatal clinic patients 9 3 HIV prevalence by sex and age group, South Africa, 2005 19 Shisana et al. (2005) 4 The HIV life cycle 25 © Wiley Interactive Concepts in Biochemistry (2005), John Wiley & Sons Inc. 5 Viral load and CD4 cell counts over time 27 6 Needle-sharing 47 © Ed Kashi/Corbis 7 Warwick Junction 49 © Stephane Vermeulin 8 Total registered deaths by age and year of death, South Africa 58 Mortality and Causes of Death in South Africa, 1997–2003: Findings from Death Notification, Statistics SA (February 2005) 9 Altered population structure due to HIV/AIDS, Botswana 64 10 The Kamitondo Youth Coffin-Making Cooperative in Kitwe, Zambia 76 © Gideon Mendel/Corbis 11 Orphanage in Cape Town, South Africa 82 © Gideon Mendel/Corbis 12 AIDS drug policy flip-flop 90 © Zapiro 13 AIDS poster 105 © Film Archive 15 World prices per patient per year for simple antiretroviral treatment 110 14 Adult mortality trends in the USA 109 Centers for Disease Control and Prevention The publisher and the author apologize for any errors or omissions in the above list. If contacted they will be pleased to rectify these at the earliest opportunity. List of tables Table 1 Regional HIV and AIDS statistics, 2003 and 2005 7 UNAIDS, Global Epidemic Report 2006 Table 2 Incidence and prevalence 16 Table 3 Routes of exposure and risk of infection 30 Adapted from R. A. Royce, A. Seña, W. Cates, and M. S. N. Cohen, ‘Current Concepts: Sexual Transmission of HIV’, New England Journal of Medicine, 336 (10 April 1997): 1072–8 Table 4 Estimated and projected impact of HIV/AIDS on mortality indicators 62 World Population Prospects: The 2002 Revision, CD-ROM (United Nations, Department of Economic and Social Affairs, Population Division publication) Table 5 Locating appropriate responses 114 This page intentionally left blank Chapter 1 The emergence and state of the HIV/AIDS epidemic The identification of HIV/AIDS Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV), which crossed from primates into humans. Although isolated cases of infection in people may have appeared earlier, the first cases of the current epidemic probably occurred in the 1930s, and the disease spread rapidly in the 1970s. AIDS was publicly reported on 5 June 1981, in the Morbidity and Mortality Weekly Report produced by the Centers for Disease Control (CDC) in Atlanta in the USA. Doctors recorded unexpected clusters of previously extremely rare diseases such as Pneumocystis carinii, a type of pneumonia, and Kaposi’s sarcoma, a normally slow-growing tumour. These conditions manifested in exceptionally serious forms, and in a narrowly defined risk group – young homosexual men. It soon became apparent that these illnesses were occurring in other definable groups: haemophiliacs, blood transfusion recipients, and intravenous drug users (IDUs). By 1982, cases were being seen among the partners and infants of those infected. The name: acquired immunodeficiency syndrome, acronym AIDS, 1 was agreed in Washington in July 1982. In the same year the CDC produced a working definition for AIDS based on clinical signs. AIDS describes the disease accurately: people acquire the condition; it results in a deficiency within the immune system; and it is a syndrome not a single disease. In French, Portuguese, and Spanish, it is known as SIDA, the full French name being syndrome d’immunodéficience acquise. HIV/AIDS Beyond North America, there was news of cases from Europe, Australia, New Zealand, Latin America, especially Brazil and Mexico, and Africa. In Zambia, a significant rise in cases of Kaposi’s sarcoma was recorded. In Kinshasa in the Democratic Republic of the Congo, there was an upsurge in patients with cryptococcosis, an unusual fungal infection. The Ugandan Ministry of Health was receiving reports of increased and unexpected deaths in Lake Victoria fishing villages. Even when the syndrome had been identified and named, it was not clear what its cause was, how it spread, or which treatments were effective or could be developed. Scientists agreed the most likely origin was a, then unidentified, virus. The hunt for this was intense in laboratories across the world, with international collaboration, and sharing of specimens and tissue. In 1983 the virus was identified by the Institut Pasteur in France, which called it Lymphadenopathy-Associated Virus, or LAV. In April 1984 in the US, the National Cancer Institute (NCI) isolated the virus and named it HTLV-III. There was an unseemly spat when the US Secretary for Health and Human Services announced to the world that the NCI was responsible for the scientific breakthrough that identified HIV. The face-saving compromise was to say French and US laboratories had both identified the cause of AIDS. In 1987 the name ‘human immunodeficiency virus’ was confirmed by the International Committee on Taxonomy of Viruses. Many diseases spread from animals to humans (and the other way). These are called zoonoses. Recent examples include severe 2 acute respiratory syndrome (SARS), which was tracked to civet cats, and avian influenza (bird flu). HIV is, so far, the most deadly pathogen to have made this leap: Ebola virus is more infectious but can be contained; SARS, fortunately was, not as infectious; avian flu has not yet taken hold in humans, but is cause for concern. Having identified how HIV was spread, the challenge was to reduce transmission. Early responses were technical: improving blood safety, providing condoms, and encouraging safe injecting practices. Soon it became apparent that these were not enough, behaviours needed to change. At the same time, the race was on to find drugs that could cure or, at least, treat infected people. It took 15 years to develop effective antiretroviral therapies (ART), and this advance was announced at the 1996 International AIDS Conference in Vancouver. There is still little understanding of the long-term impact of the epidemic. While the worst predictions: of national collapse, rising levels of crime, economic stagnation, and general malaise 3 The emergence and state of the HIV/AIDS epidemic Initially there was a degree of hysteria around AIDS, where it came from, and how it was transmitted. In San Francisco, when it was identified as a gay men’s disease, police and fire officers feared they would be infected through exposure to blood and body fluids from homosexuals. In 1983 officers were given face masks and gloves and educated on how to protect themselves from this alleged risk. Today, when AIDS hits the headlines in the West, which is not often, most stories fall into a few categories: what the West (and Western celebrities) are doing to assist the worst affected countries and communities, such as supporting orphanages and adopting orphans; the impoverishment and misery AIDS causes; the continued spread among certain groups – IDUs in the former Soviet countries or Chinese peasants; and, in rich countries, the deliberate spreading of the virus by individuals to implicitly ‘innocent victims’. won’t come about, vulnerabilities, like the epidemic, will be differentiated. The poorest bear the burden. The long-wave epidemic HIV/AIDS AIDS is new: in 2006, the 25th anniversary of its identification, there were close to 40 million people around the world living with HIV and over 20 million had died. Globally the number of infections had increased rapidly. This growth has slowed but continues steadily, however it is confined to specific locations; the feared uncontrollable worldwide pandemic has not occurred. The virus itself is unusual, as explained in detail in the next chapter. The most common mode of transmission is sexual intercourse, followed by mother-to-child infection, sharing drug-injecting equipment, and contaminated blood or instruments in health care settings. Because transmission is mainly through sex or drug use and there is no cure, there is much prejudice and fear. HIV/AIDS was and remains stigmatizing at an individual and national level. HIV/AIDS is a complex long-wave event: there are waves of spread and waves of impact. This concept is illustrated by the three curves shown in Figure 1. The first shows the prevalence rising steadily and levelling off, a silent spread. The second curve, six to ten years later, is the cumulative number of AIDS cases. These are visible but diffused across a nation, and each year the numbers are small. Those studying HIV know infections will develop into illnesses and, untreated, lead to death. At T1 the number of cases at T2 can be predicted and should be planned for. The third curve, even further in the future, is the impact, which is harder to predict and plan for. Some idea of the timescale comes from Uganda. Here HIV prevalence peaked in about 1989, and the number of AIDS 4 Prevalence A A1 A2 Cases B B1 Impact Time 1. Epidemic curves orphans peaked 14 years later in 2003. In countries such as South Africa, where HIV prevalence may not have peaked, the number of orphans could still be rising in 2020. Orphaned children carry the effects of being orphaned for the rest of their lives. Impacts last for generations. The diagram shows three of the waves; there will be others and the impact will be long term. The future of HIV/AIDS is, epidemiologically speaking, reasonably predictable. Unless the virus mutates and becomes more easily transmitted, it will be contained. Science is advancing and new treatments are becoming available. Technological prevention methods, such as microbicides and vaccines, are being developed, although these are still some years away. The impacts are less certain, but will be confined to the worst affected regions, notably parts of Africa; and most marginal groups. Due to the specific demographics of declining and ageing populations, some Eastern European countries may be particularly adversely impacted. 5 The emergence and state of the HIV/AIDS epidemic T2 T1 The global and regional epidemics HIV/AIDS This part of the chapter reviews the worldwide epidemic mainly using data from the 2006 biannual UNAIDS Report on the Global AIDS Epidemic. HIV has not spread uniformly. Although most early reported cases were among gay men in the USA and Europe, the greatest numbers have consistently been African. In 1980 there were about 18,000 HIV infections in North America, 1,000 each in Europe and Latin America, and 41,000 in sub-Saharan Africa. Table 1 shows current data. There are different sub-epidemics around the world. Southern Africa has an epidemic transmitted primarily through heterosexual intercourse, with more women than men infected. In Asia total numbers are alarming but small as a proportion of the populations. The East European and central Asian epidemics have been principally fuelled by IDUs and are growing. In rich countries the epidemic is contained, and mainly seen among marginal groups, although numbers are slowly rising. Sub-Saharan Africa has the largest number of people living with HIV: two-thirds (64%) of infected people and three-quarters of all infected women live here. There are differences in the sizes and trajectories of African epidemics. Southern Africa has the worst epidemic, with the numbers infected still rising in some countries. South Africa’s antenatal clinic survey recorded an increased prevalence from 29.5% in 2004 to 30.2% in 2005, but this fell to 29.1% in 2006, and there are other hopeful signs: data from Zimbabwe and Zambia also suggest a fall in prevalence. In Zimbabwe, HIV prevalence in pregnant women fell from 26% in 2002 to 21% in 2004, and in younger women (15–24) the drop was from 29% to 20% between 2000 and 2004. In most of West Africa, HIV seems not to have spread. Senegal is held as a model for successful prevention: HIV prevalence was below 1% throughout the 1980s and 1990s, increasing slightly to 6 Table 1. Regional HIV and AIDS statistics, 2003 and 2005 Country Adults (15+) and Adults (15+) children and children newly living with infected HIV with HIV Adults (15–49) prevalence (%) Adult (15+) and child deaths due to AIDS Sub-Saharan Africa 24.5 million 2.7 million 6.1 2.0 million 2003 23.5 million 2.6 million 6.2 1.9 million North Africa and Middle East 2005 440 000 64 000 0.2 37 000 2003 380 000 54 000 0.2 34 000 Asia 2005 8.3 million 930 000 0.4 600 000 2003 7.6 million 860 000 0.4 500 000 Oceania 2005 78 000 7 200 0.3 3 400 2003 66 000 9 000 0.3 2 300 140 000 0.5 59 000 Latin America 2005 1.6 million 7 The emergence and state of the HIV/AIDS epidemic 2005 Table 1. (Continued) Country Adults (15+) and Adults (15+) children and children newly living with infected HIV with HIV Adults (15–49) prevalence (%) Adult (15+) and child deaths due to AIDS 2003 1.4 million 130 000 0.5 51 000 Caribbean 2005 330 000 37 000 1.6 27 000 2003 310 000 34 000 1.5 28 000 HIV/AIDS Eastern Europe and Central Asia 2005 1.5 million 220 000 0.8 53 000 2003 1.1 million 160 000 0.6 28 000 North America, Western and Central Europe 2005 2.0 million 65 000 0.5 30 000 2003 1.8 million 65 000 0.5 30 000 TOTAL 2005 38.6 million 4.1 million 1.0 2.8 million 2003 36.2 million 3.9 million 1.0 2.6 million 8 HIV antenatal prevalence in southern African countries Percentatge prevalence 45 40 35 30 25 20 15 Botswana 10 South Africa 5 Namibia Lesotho Swaziland 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2. Southern African epidemics: HIV prevalence in antenatal clinic patients 1.1% in 2002 and falling back to 0.9% in 2005, although increases in prevalence are being reported from some specific groups such as migrant men. In East Africa, prevalence peaked and is declining. Behavioural data show this is due to increased condom use in casual relationships; reduction in numbers of partners; and delayed sexual debut. The greatest reduction is in Uganda, which, in the 1980s, was the global epicentre of the epidemic: at the peak in 1990, HIV prevalence may have been 31% among pregnant women; it was believed to be just 4.7% in this group in 2002. In North Africa and the Middle East, although there is little evidence of HIV, there is concern about high risk factors. Sexual intercourse is the dominant form of transmission but there are signs of spread among drug users. Stigma and discrimination are particularly marked here and mean the epidemic remains hidden. 9 The emergence and state of the HIV/AIDS epidemic 0 HIV/AIDS In the Caribbean and Latin America, numbers are rising slowly overall. In the Caribbean, spread is predominantly heterosexual and concentrated in identifiable groups such as sex workers, although there is evidence of slow movement to the broader population. Women comprise 51% of adults living with HIV here. The worst epidemic was in Haiti, but prevalence fell from 6.2% in 1993 to 3.8% in 2006. Cuba has consistently kept its prevalence very low, less than 0.1%. Its prevention methods flew in the face of human rights and are discussed in Chapter 7. Latin America’s epidemic is concentrated among populations at particular risk, and the majority of infections are the result of contaminated drug-injecting equipment or sex between men, whereas in Central America, the virus is spread predominantly through heterosexual sex. In Eastern Europe, the number of HIV infections, being driven primarily by IDUs, has risen dramatically, reaching 1.5 million at the end of 2005. Prior to 1990, there were few infections, and most of those affected were foreigners. The most serious epidemic proportionately is in Ukraine. Here, between 1987 and 1994, some 39 million tests were done and only 398 cases of HIV were detected, of which 54% were foreign. The epidemic took off in 1995, when 1,489 infections were identified, of which 99.4% were Ukrainian and 68.6% were IDUs. By the end of 2005, an estimated 410,000 people were infected, an adult prevalence rate of 1.4%. Ukraine’s epidemic continues to expand, and newly registered HIV infections increased by 25% in 2002. The Russian Federation has the highest number of infections: an estimated 940,000 people. Between 1.5 and 3 million Russians are believed to inject drugs (1% to 2% of the entire population). In the Baltic states of Belarus and Moldova, transmission is increasing, although overall the numbers remain low. Intravenous drug use accounts for the largest proportion of newly reported infections but sexual transmission is slowly gaining ground. 10 HIV prevalence is low (less than 0.3%) in most of Central Asia and the Caucasus, though numbers are rising. The epidemic is recent: in Uzbekistan, reported infections rose from 28 in 1999 to 2,016 in 2004. Given that the epidemic is located in core transmitter groups – IDUs and sex workers – it might be halted with prevention strategies concentrating on those most at risk. However, coverage is low: 10% of sex workers, fewer than 8% of IDUs, and 4% of men who have sex with men are reached by prevention messages. Thailand seemed set to experience a large epidemic, between late 1987 and mid-1988 prevalence rose from 0 to more than 30% among IDUs in Bangkok. Prevalence among sex workers was between 1% and 5% in various locations in 1989, but in the city of Chiang Mai it was 44%. The government reaction was immediate and forceful: efforts were mounted to promote condom use, reduce risky behaviour, treat STIs, and provide care. A cornerstone of the response was the ‘100% condom programme’, which required consistent condom use in brothels. Early indicators of success were increased condom use from 14% to over 90% by 1992 in brothels, and a decrease in episodes of male STIs at government clinics from 200,000 in 1989 to 20,000 in 11 The emergence and state of the HIV/AIDS epidemic In Asia, HIV infection levels are low, but large populations translate this to huge numbers of HIV-positive people. Some 8.3 million people are infected here, the largest number in India. The pace and severity of Asia’s epidemics vary. Some countries responded quickly and effectively, while others are experiencing expanding epidemics and need to mount responses. Indonesia, Nepal, Vietnam, and several provinces in China, Bangladesh, Laos, Pakistan, and the Philippines have extremely low levels of HIV. HIV spread in China is attributable to IDUs, paid sex, and pooling of blood among donors for transfusion. In India, Indonesia, Myanmar, and Vietnam, drug use is an important driver. HIV/AIDS 1995. HIV prevalence among pregnant women peaked at 2.35% in 1995, and declined to 1.18% in 2003. Prevalence among military conscripts decreased from 4% in 1993 to 0.5% in 2003. However, the HIV prevalence among IDUs remained high at 33% in 2003. The epidemic is largely under control in the developed world. In 2005, there were 65,000 new infections in this region, raising the number of people with HIV to 2 million. Widespread access to life-prolonging ART meant that the number of AIDS deaths was just 30,000 in 2005. Sex between men and, to a lesser extent, intravenous drug use are the predominant routes of transmission, but patterns are changing and new populations are being affected through unprotected heterosexual intercourse. In the United States, the epidemic is increasingly located among African Americans (over 50% of new HIV diagnoses in recent years have been made in this group) and is affecting greater numbers of women (African American women account for 72% of new HIV diagnoses). In Canada, indigenous populations are disproportionately infected. In 12 Western European countries with data for new infections, HIV diagnoses in people infected through heterosexual contact increased by 122% between 1997 and 2002, and most originated from countries with generalized epidemics in sub-Saharan Africa or the Caribbean. Key features of the epidemic A number of points can be drawn from this brief survey. There are differences between and within countries in terms of the size, timing, and location of the epidemics, they are not homogeneous; prevalence rates have risen to levels believed impossible a decade ago; and the epidemic does not respect national borders. The timing varies. Where the epidemic was reported early, such as in Uganda and Thailand, by 1990 HIV prevalence had peaked and was declining; whereas in Southern Africa, HIV did not begin 12 spreading among the general population until the 1990s, and in the former Soviet Union, a rapid increase in prevalence began in the late 1990s. In some countries HIV has plateaued, although deaths may have been simply replaced by new infections. In other settings the small numbers of infections in particularly vulnerable populations are remaining stable. Given the ‘right’ change in circumstances, a broader spread might occur. Location refers both to physical geographic (spatial) location and particular population groups. There are epidemic hotspots. For example, in Brazil national prevalence is well below 1%, but in some cities infection levels of over 60% have been reported among IDUs. African prevalence is higher in urban areas, near major transport routes, and at trading centres than in the rural areas, and some of the highest localized prevalence rates have been recorded at border posts. Sometimes clearly defined groups can be identified, usually those on the margins of society and who face legal or social stigmatization: sex workers, drug users, and men who have sex with men. In China’s central provinces many cases are due to the sale of blood. Peasants sold their blood, the plasma was extracted, and what was left was pooled and transfused back, a practice that prevented anaemia in the donors but ensured rapid spread of HIV, hepatitis, malaria, and other blood-borne diseases. In other provinces of China there is primarily an IDU-driven epidemic. 13 The emergence and state of the HIV/AIDS epidemic The maximum possible extent of the epidemic is uncertain. In 2002, UNAIDS, reporting on Southern Africa, noted that HIV prevalence had reached levels ‘considerably higher than had previously been thought possible’. There is a ‘natural limit’ beyond which prevalence will not grow, when everyone who is likely to be infected has been. The highest national prevalence recorded so far was Swaziland’s 42.6% among antenatal clinic patients in 2004; in 2006, prevalence had fallen to 39.2%. HIV/AIDS The international dimension of the epidemic is not always appreciated. It can be illustrated with two examples. In South East Asia, the ‘golden triangle’ is the main opium-producing area and covers the mountainous region where Myanmar, Laos, and Thailand meet and has links into southern China, the states of eastern India, and northern Vietnam. Drugs are a major illegal export and the area is home to many addicts and hence infected people. If the golden triangle were a country, it would have a high prevalence and be a major source of concern to ‘its’ government. The second example concerns the UK, where, since 1996, there have been 29,357 HIV diagnoses. Year after year the number of new diagnoses has risen steadily, from 2,014 in 2000, to 4,474 for 2003, the last year for which there are complete data (the Health Protection Agency reports 4,287 cases in 2004 but expects numbers to rise as more data are received). The vast majority of new HIV infections worldwide – 92.5% – were heterosexually contracted. Of these, 78.6% were infected in the developing world, most in Southern and Eastern Africa. Some of these people are political or economic refugees, others have been recruited to work in fields with skills shortages. Migration and refugee flows are contributing to the continued increases in HIV prevalence in many European countries. It is a complex and difficult problem, and reaffirms HIV/AIDS as a global dilemma even for countries where prevalence is low. Key concepts: prevalence and incidence Prevalence and incidence are key concepts in epidemiology and are important for understanding the spread of HIV and associated data. Prevalence is the absolute number of people infected. The prevalence rate is the proportion of the population that has a disease at a particular time (or averaged over a period of time). With HIV, prevalence rates are given as a percentage of a specific 14 segment of the population, for example adults aged between 15 and 65, antenatal clinic patients, blood donors, or an ‘at risk’ group. HIV prevalence data come from surveys: in the early years, surveys were done among blood donors, STI clinic patients, people with TB, and pregnant women. Incidence is the number of new infections over a given period of time. The incidence rate is the number per specified unit of population (this can be per 1,000, per 10,000, or per million for rare diseases) and period of time (in the case of cholera, for example, this can be per day or week). Measuring HIV incidence is complex and expensive. Where information comes from In the early days AIDS cases caught the headlines and provided an indicator of the spread. The number of people falling ill and dying rose relentlessly; no one knew who was at risk or how far the disease would spread. Each country counted the number of AIDS cases and sent this information to the World Health Organization (WHO), which then reported on the state of the global pandemic. AIDS case data are no longer routinely collected, except in well-resourced countries. The most commonly used and reported information is HIV prevalence; the estimated number 15 The emergence and state of the HIV/AIDS epidemic People infected with HIV remain so for the rest of their lives; the only way they leave the pool of HIV infections is to die. This means the prevalence can continue rising even after the incidence has peaked, and the introduction of ART makes understanding data more complex as people live longer. This is explored in Table 2. In this example, incidence peaks in year 6, and prevalence continues to rise, then the introduction of ART in year 9 means that it rises even more rapidly. Table 2. Incidence and prevalence Year Population Incidence (actual) Incidence rate per 1000 Prevalence 1 9 750 0 2 10 000 50 5 3 10 250 50 4 10 500 5 Deaths of Prevalence infected rate (%) people 0 Comments Year zero 50 0.5 4.8 100 0.97 Slow increase 150 14.3 250 2.3 Exponential 10 750 550 51 750 6.9 200 6 11 000 700 68 1150 10.5 300 7 11 250 650 57.7 1400 12.4 400 8 11 400 600 52.6 1550 13.6 450 9 11 400 400 35 1750 15.4 200 10 11 300 300 26.5 1850 16.4 200 Peak incidence ART introduced Data sources The best source of information, other than looking at each country individually, is UNAIDS, which produces a biannual report including a statistical annex. These data are mainly based on what is collected and reported by each country. This gives rise to problems, and in some instances, we simply do not know what the situation is. There are few data from states in conflict, such as the Democratic Republic of the Congo or Sudan, or those without a functioning government to collect, collate, and disseminate information, for example from surveys done in 2001, at only 10 urban and 70 rural sites. In Zimbabwe it is hard to believe reliable HIV data are being collected as the health system is overstretched and the economy is collapsing. Data are sensitive. UNAIDS was unable to publish an estimate of the numbers of people infected with HIV in India in 2004 as the government would not agree to a figure (although they were allowed to put in an estimate: 2,200,000 to 7,600,000 infections). In July 2007, new estimates were released by the Indian Government, UNAIDS, and the WHO, putting the figure at between 2 and 3.1 million infections. For political reasons, the UN finds it difficult to make negative comments on the quality of the data with which they are presented. The 2006 UNAIDS report notes the global estimates of people living with HIV/AIDS are lower than previously reported. This is because of genuine declines in prevalence 17 The emergence and state of the HIV/AIDS epidemic Afghanistan and Somalia. Data may simply not be credible due to inefficiency and government failure. An example is Nigeria: data reported by UNAIDS in 2006 for Nigeria came in some settings and because new data are available from population-based surveys. The 2006 report looks at all adults, whereas previously only those aged 15 to 49 were included. More HIV-infected people are living beyond 50, and ART will increase this further. HIV/AIDS of infections; and the number of orphans due to AIDS. HIV prevalence is given as the percentage of those infected of all adults (until recently this was given as people between the ages of 15 and 49). The most consistent prevalence data come from women in antenatal clinic (ANC) surveys. Originally this population was chosen because they provided the best sample: blood was routinely taken for other tests; the women had been sexually active; and the surveys could be done on an anonymous basis, meaning the sample could not be linked to individual women, so informed consent was not required. ANC data give a reasonable picture of the epidemic provided biases are recognized. The main biases are that men are excluded; younger women are over-represented (as they are more sexually active and likely to fall pregnant); HIV-positive and older women are under-represented as HIV infection and age reduce fertility; and surveys usually draw on women attending public antenatal clinics. This last point means women who are too poor to access the government clinics and also those who get private health care will be excluded. Once data are available, it is possible to estimate the number and percentage of all women, men, and adults who are infected, as well as the number of children who will be born HIV positive, by 18 using models that adjust for the biases. Some models are in the public domain and accessible through the Internet. Two population surveys in South Africa were carried out for the Nelson Mandela Foundation by the Human Sciences Research Council, in 2002 and 2005. The entire population, except children under 2, were sampled. The 2002 survey found a prevalence rate of 17.7% among women aged 15–49. By 2005, it had increased to 20.2%. The survey allows us to locate the epidemic by age and gender, as shown in Figure 3. This figure is typical of the 35 Percent 30 Male 25 Female 20 15 10 5 0 2--14 15--19 20--24 25--29 30--34 35--39 40--44 45--49 50--54 55--59 60+ Age Group 3. HIV prevalence by sex and age group, South Africa, 2005 19 The emergence and state of the HIV/AIDS epidemic New data are becoming available through population-based surveys of HIV prevalence, which collect nationally representative information on HIV prevalence and provide data on characteristics associated with infection and risk. Most have been done as part of the Demographic and Health Surveys (DHS). Since 2001 there have been 13 surveys carried out and published by the US-based Macro International Inc., and a further 20 are in various stages of completion at the time of writing in 2007. A comparison between the recent DHS results and UNAIDS estimates showed that in three cases UNAIDS estimated adult prevalence was higher, in four instances lower, and in the remaining six the rates were the same. Both DHS and ANC data sets can be used provided they are treated with care. HIV/AIDS heterosexual epidemics. If a graph of prevalence were drawn for Russia, it would show more men than women infected, as their epidemic is being driven by IDUs. In addition to surveys among ANC patients, specific risk groups, and population-based studies, there are other data sources. Most common are of specific occupations such as the military, teachers, health workers, and employees of particular companies (although these may not be in the public domain). A survey of teachers in South Africa in 2005 showed HIV prevalence was highest in the 25–34 age group (21.4%), followed by the 35–44 age group (12.8%). This has policy implications, as teachers are crucial for economic and social development. In Nigeria, HIV prevalence among army troops was estimated to be less than 1% in 1989/90, it increased to 5% in 1997, and 10% in 1999. Among Nigerian troops in Sierra Leone, prevalence increased from 7% after one year to more than 15% after three years of duty in the operational area. In Botswana, Debswana, the diamond-mining company, carried out its first survey in 1999 and found HIV prevalence across all employees was 28.8%. The company decided to provide ART for staff and spouses, re-target their prevention programmes, and require ‘AIDS compliance’ from contractors. They maintained their policy of testing scholarship applicants for long-term training abroad and refusing those who were HIV positive. The 2003 survey showed HIV prevalence had fallen to 22.6%: in permanent employees it was 19.9% and among contract employees 28.3%. Conclusion In 2006 there were cautious suggestions that global HIV incidence might have peaked, perhaps even in the late 1990s. The 2006 UNAIDS epidemic report revised the global number of 20 people living with HIV slightly downwards from its 2005 figures. However, HIV data must be seen against a backdrop of the three curves (see Figure 1). In 2002, it was estimated that HIV/AIDS caused 4.9% of deaths globally and a quarter of all deaths from infectious and parasitic diseases. The WHO estimates that in 2015 AIDS will still cause one in six deaths in Africa. The emergence and state of the HIV/AIDS epidemic 21 Chapter 2 How HIV/AIDS works and scientific responses AIDS appeared at a time when the world was growing ever more interconnected, one of the reasons it spread so rapidly. It also came at a point of unprecedented scientific advance and confidence. The eradication of smallpox in 1977, advances in virology and immunology and in a range of other medical disciplines had given rise to optimism about what science and medicine could do. Although there was the science available to understand its origins and the mechanisms of HIV and AIDS, it soon became clear there was to be no medical or scientific silver bullet. Preventing HIV transmission and successfully treating patients needs more than scientific solutions. The epidemic has found its most fertile locations in parts of the world where there is poverty and inequity, especially where this is gendered. Dealing with this disease means understanding the science and then looking beyond it. How the virus works There are two main sub-types of the virus: HIV-1 and HIV-2, the latter being harder to transmit and slower-acting. Both originate in simian (monkey) immunodeficiency viruses (SIV) found in Africa. The source of HIV-1 was chimpanzees in Central Africa, while HIV-2 derived in West Africa from sooty mangabey 22 monkeys. How and when the virus crossed the species barrier continue to be sources of speculation and historical interest. Current thinking is that the epidemic had its origins through chimpanzee and monkey blood entering people’s bodies possibly during the butchering of bush meat in the 1930s. The genetic material of life forms, including most viruses, is deoxyribonucleic acid (DNA). This contains the genetic instructions specifying the biological development of cellular life. Some viruses, including HIV, have ribonucleic acid (RNA) as their genetic material, and are called retroviruses (scientifically, retroviridae). HIV also belongs in the family of viruses known as lentiviruses, which means slow-acting. In humans, lentiviruses result in diseases that develop over a long period, many affecting the immune system and brain. HIV has to invade cells to reproduce. Within these cells, it produces more virus particles by converting viral RNA into DNA in the cell and then making many RNA copies. The conversion is done through an enzyme called reverse transcriptase. The switch from RNA to DNA and back to RNA is significant and makes combating HIV difficult. Each time it occurs there is a possibility of errors and the virus mutating. This is made more likely because reverse transcriptase lacks the normal ‘proofreading’ that occurs with DNA replication. Once formed, the copies or virus particles break out of the cell, destroying it and infecting other cells. 23 How HIV/AIDS works and scientific responses Viruses have been described as ‘a piece of nucleic acid surrounded by bad news’. A virus is genetic material covered with a coat of protein molecules. Viruses do not have cell walls, are parasitic, and can only replicate by entering host cells. They have few genes compared with other organisms: HIV has fewer than 10 genes; the smallpox virus has between 200 and 400 genes; the smallest bacterium has 5,000 to 10,000 genes; and humans have about 30,000 genes. HIV/AIDS The mutation of the virus means various sub-types or clades of virus have evolved. Identifying clades allows scientists and epidemiologists to track the spread of infection across the world. Type B is the main clade in the USA, type C in Southern Africa, while in East Africa, A and D are most common. The greatest variety is in West Central Africa. Mutation means the virus can outwit human responses, both our biological response and the technology we deploy through drug development. Individual human immune systems fight infections, and we can pass this resistance and response on to the next generations. However, HIV attacks the cells of the immune system and, in particular, CD4 cells. There are two main types of CD4 cells. The prime target is CD4 T cells which organize the body’s overall immune response to foreign bodies and infections. The virus also attacks immune cells called macrophages which engulf foreign invaders in the body and ensure the immune system will recognize them in the future. Once the virus has penetrated the wall of the CD4 cell it is safe because it has become part of the immune system. The biological response of ‘herd immunity’, where the ability to fight an infection is passed on, or succeeding generations are ‘selected’ because they are resistant to a disease, does not yet occur with HIV. Virus particles lie dormant in the cells until their replication is triggered. The trigger is not fully understood but could be an infection such as TB, or the deterioration of the immune system. The process of viral insertion, transcription, and particle expulsion is shown in Figure 4. Our technological response is limited. The virus mutates and becomes resistant to drugs. For an individual, this means the drug combination they take should be tailored to the variant of virus with which they are infected. A person developing drug-resistant HIV infection in the rich world requires costly tests, sophisticated 24 laboratory facilities, and drug combinations; in the poor world, it is usually a death sentence. At the population level, drug-resistant infections have long-term ramifications; if they spread, treatment becomes much more difficult and expensive for everyone. HIV mutation may mean it becomes less of a killer, but equally it could become more robust and easily transmitted. Virologists monitor the virus and its changes to ensure we are warned of new developments. While it is generally understood that HIV infection is for life, what is often not appreciated is that an HIV-infected person can be re-infected with new strains of the virus, damaging their prospects for survival. Effectively, such individuals get ‘super-infections’. When a person is newly infected, they sero-convert – this means the virus has taken hold in the body and it (or its antibodies) will be detectable by an HIV test. During this period, an infected 25 How HIV/AIDS works and scientific responses 4. The HIV life cycle Testing Most HIV tests look for the presence of antibodies to the virus rather than detecting the virus itself: if a person has antibodies, they have the virus. The most common test for antibodies is the enzyme-linked immunosorbent assay (ELISA), which is cheap and simple to perform. Initially, HIV could only be detected using blood samples. The South African and the DHS surveys described in Chapter 1 collected people’s blood on absorbent paper by pricking a finger, heel, or ear. This is invasive, as people don’t like having blood taken, but it is as simple as the process many diabetics go through daily to assess their blood-sugar levels. However, there are now tests that can identify the antibodies in saliva HIV/AIDS and other body fluids and they are quick and easy to use, especially in the context of population surveys. Tests have also been developed to estimate how recently a person has been infected, giving a measure of incidence. Although the indirect tests such as ELISA are cheaper and quicker than testing for the virus itself, testing for the virus is sometimes preferable and involves a process called polymerase chain reaction (PCR). This uses a technique by which DNA from a cell can be replicated to a point when it can be measured. Both ELISAs and PCRs are also used for detection of diseases other than HIV. person may experience a flu-like illness and will have very high viral loads, that is the number of virus particles in the blood or body fluids, especially semen or vaginal secretions, will be high. However, there is a ‘window’ period when a person may be infected and infectious but the virus is not yet detectable, meaning HIV tests are not completely reliable for new infections, and blood supply safety cannot be guaranteed. In the period 26 immediately after infection, a person will be very infectious. This is of epidemiological importance. The more people there are in the early stage of infection, the greater the chance of exposure and infection, thus the epidemic builds up its own momentum. Infectivity also rises as the disease progresses and the viral load increases. 1200 1100 1000 900 800 700 600 500 400 300 200 100 0 Primary Infection Clinical Latency Death Opportunistic diseases 1/512 1/256 1/128 1/64 1/32 1/16 1/8 1/4 1/2 0 3 6 9 12 Weeks 1 2 3 4 5 6 7 8 Years 5. Viral load and CD4 cell counts over time 27 9 10 11 Culturable Plasma Viremia (dilutional titer) CD4 Lymphocyte Count (cells/mm3) The World Health Organization recognizes four stages in HIV disease progression. Stage 1 is asymptomatic infection, when the CD4 count is normally greater than 500 per mm3 of blood. How HIV/AIDS works and scientific responses The window period is followed by the long incubation stage. During this phase, the viruses and the cells they attack are reproducing rapidly and are being wiped out as quickly by each other. Every day up to 5% of the body’s CD4 cells (about 2,000 million cells) may be destroyed by approximately 10 billion new virus particles. Eventually, the virus destroys immune cells more quickly than they can be replaced. A healthy CD4 cell count is normally over 1,000 cells per mm3 of blood. As infection progresses, this number falls, as shown in Figure 5. HIV/AIDS Stage 2 is when the count is between 350 and 499 per mm3, and symptoms might include some mild weight loss, fungal infections, and herpes zoster (shingles). When the CD4 cell count falls below 350, in stage 3, a person has advanced immunosuppression with opportunistic infections, fevers, severe weight loss, diarrhoea, candidiasis (infection with a yeast-like fungus that causes thrush), and possibly TB. Stage 4, AIDS, occurs when there are fewer than 200 CD4 cells per mm3 of blood and the person is seriously ill with diseases such as TB which may spread beyond the lungs, Pneumocystis carinii and other pneumonias, the parasitic disease toxoplasmosis, and meningitis. A few people may experience symptoms of disease with CD4 counts above 200, while others show no symptoms with CD4 counts below 200. Generally though, infections will increase in frequency, severity, and duration until the person dies. The CD4 count is one of the measures used by physicians in deciding when to begin drug therapy. Transmission HIV is found in all body fluids of an infected person, although in minimal quantities in sweat, tears, and saliva. Exposure to blood or blood products carries the maximum risk of infection. This is why there is so much concern around blood safety and hygiene in health care settings, and why there are high levels of transmission among drug users who share syringes. However, sexual intercourse is the most common source of transmission: 75–85% of people are infected this way. This includes both homosexual and heterosexual intercourse, though globally heterosexual intercourse predominates. The virus can be passed from infected mothers to their infants by crossing the placenta, during the birth process, and through breast milk. Reducing the risk prior to or during birth is simple: in most resource-poor settings, the drug nevirapine is used, which 28 The comparative efficiency of different modes of transmission is shown in Table 3. The chance of infection varies with stage of disease, and the viral load is crucial. Also important is the state of the immune system, health, and nutritional status of the exposed person. One benefit of ART is that it reduces the viral load, making a person on treatment much less infectious. There is a debate as to whether treatment will increase or reduce the scale of the epidemic. Reduced viral loads reduce infectivity, but the infected person is around for longer, and may be more sexually active; on the other hand, people on treatment may want to protect themselves and others. There is no clear evidence on this yet. Treatment The period from infection to illness is, on average, about eight years. This can be extended with basic lifestyle changes; a person who eats properly, does not smoke, take drugs, or excessive amounts of alcohol, and gets regular exercise will live a longer and healthier life. Immune system boosters, including some indigenous and herbal preparations, can help prevent opportunistic infections and prolong life. 29 How HIV/AIDS works and scientific responses lowers mother-to-child transmission from about 25% to between 8% and 17%. The drug is cheap and easily administered, with one dose for the mother prior to delivery and a dose for the infant after birth. Where affordable, more complex treatments, including ART, are offered, and are so successful that few babies are born with HIV infection. If mothers have access to clean water and infant feeding formula, then bottle-feeding means HIV will not be transmitted through breast milk. However, in many settings this is not the case, and work at the University of KwaZulu-Natal has shown that where formula and clean water are not available, babies of women who exclusively breast-feed are substantially less likely to be infected than infants who are given both formula and breast milk. Table 3. Routes of exposure and risk of infection Infection route Risk of infection Sexual transmission Female-to-male transmission 1:700 to 1:3000 Male-to-female transmission 1:200 to 1:2000 Male-to-male transmission 1:10 to 1:1600 Fellatio 0 to 6:100 HIV/AIDS Parenteral transmission Transfusion of infected blood 95:100 Needle-sharing 1:150 Needle stick 1:200 Needle stick/AZT PEP 1:10000 Transmission from mother to infant Without AZT treatment 1:4 With AZT treatment Less than 1:10 There has been considerable debate on the importance of nutrition. A WHO-led consultation in Durban in 2005 confirmed that infected people have greater calorific needs. Asymptomatic adults and children require 10% more energy from their diet than uninfected adults or children, and adults who have become 30 ill need 20 to 30% more energy, while sick children require 50 to 100% more. There is, as yet, no evidence of greater protein requirements among infected people, and the relationships between micronutrient supplementation and HIV/AIDS need more investigation. Complicating factors are that people suffering from HIV/AIDS often experience loss of appetite, inability to eat due to infections of the mouth and throat, and failure to properly digest food. Additionally, the loss of labour and income that results from family members becoming ill may lead to there being less food available in the household (see Chapter 5). Eventually ART is needed. These drugs reduce viral activity, allow the immune system to recover, and prolong and improve quality of life. As an illustration of their effectiveness, in the USA by 1991, HIV was the leading cause of death among adults aged 25 to 44, and rates reached close to 40 deaths per 100,000 by 1995. The introduction of ART in 1996 meant mortality plummeted, so that by 2000, it had fallen to about 10 per 100,000. Patients who had resigned themselves to death, cashed in life insurance policies, and given up employment found themselves granted a new lease of life – so dramatic it became known as the ‘Lazarus syndrome’. The first effective drug was azidothymidine, known as AZT with the trade name Retrovir. This had short-term benefits but resistance to the drug in the body developed rapidly. It was found 31 How HIV/AIDS works and scientific responses As the CD4 cell count falls and the immune system is compromised, the infected person experiences ‘opportunistic’ infections – that is, infections that would rarely affect or cause serious symptoms in people whose immune systems were healthy. Most can be treated, and the role of prophylaxis is important. An antibiotic such as cotrimoxazole prevents Pneumocystis carinii infections and other bacterial pneumonias, toxoplasmosis, and salmonella bacteraemia, and tuberculosis can be prevented with isoniazid. These treatments are cheap and effective, but do not address the underlying HIV infection. HIV/AIDS that combinations of drugs, acting in different places and on different stages of the viral replication cycle (shown in Figure 4) were most effective, and the standard treatment is currently triple therapy using three different drugs. In the wealthy world, the combination of drugs will be tailored to the needs of the patient and even the variant of the virus with which they are infected. These do not eliminate the virus from a patient’s body, and reservoirs of infection remain. If treatment ceases, the virus will emerge and begin replication again, therefore current therapies have to be taken for life. In resource-poor settings the combination of drugs offered usually includes, as a first line of treatment, two from a class called non-nucleoside reverse transcriptase inhibitors (NNRTIs) and one nucleoside reverse transcriptase inhibitor (NRTI). There is evidence suggesting this first-line therapy provides about five years of healthy life before resistance develops. When this occurs, a second line of treatment must be adopted to prolong life. The WHO recommends that second-line therapy include two NRTIs and a third class of drug called protease inhibitors (PIs). All the drugs used to treat HIV/AIDS are complex and expensive (particularly PIs, which also require special handling – refrigeration). They are also toxic. Not all patients can tolerate them, and not all drugs will work for an individual patient. The more the combinations and dosages can be adapted to the individual, the better their prognosis. Additionally, few drugs are available in paediatric formulations, which means that infected infants and children have to take adaptations of adult drugs (although this is changing). There is a debate as to the best time to begin the ART regimen. Early treatment prevents damage to the body caused by high and prolonged viral loads, but decreases options if resistance builds up. The WHO guidelines, somewhat unhelpfully, say: 32 ‘the optimum time to commence ART is before patients become unwell or present with their first opportunistic infection’. This assumes that people know their HIV status, and most don’t. The guidelines state treatment should be considered when the CD4 cell count falls below 350 and certainly started before it is 200 or lower. Where there are laboratory services available, the viral load (the number of virus particles in a person’s blood) can be monitored and, if it rises above 55,000 copies per millilitre, treatment should start. Cost is a factor. In affluent countries, where physicians tailor combinations of drugs, the total cost of treatment per patient is between US$ 850 and US$ 1,500 per month (this includes drugs, laboratory tests, and health care staff ). In 2007, the cheapest combination of drugs in the developing world was US$ 94 per patient per year. This, with associated costs of laboratory testing and health care worker time, means the lowest possible price for first-line treatment would be about US$ 250 annually. Western pharmaceutical companies are the main source of new drugs, but cheaper generic versions come from developing world manufacturers, mainly in India and Thailand, with South Africa and Brazil being recent entrants into drug manufacturing. The major purchasers of drugs are international development agencies, the American Presidential Emergency Plan for AIDS Relief (PEPFAR), the Global Fund for HIV/AIDS, TB and Malaria (Global Fund), and national treatment programmes. The prices paid vary greatly from country to country, and even within a country depending on who does the purchasing. 33 How HIV/AIDS works and scientific responses Where resources are limited, the tendency is to treat more conservatively. In South Africa, for example, national guidelines are that a person with a CD4 cell count of less than 200 should be put on ART. In most African and Asian countries this is the standard of care in public health settings. Despite recent price reductions, affordability and access remain an issue for most people in poor countries. In Uganda combined public and private spending on all health care is estimated at only US$ 38 per capita per year. The cost of ART drugs alone is US$ 28 per month, and this excludes clinical consultations, monitoring, tests, and drugs for opportunistic infections. Only wealthy people can afford medicines, and even they have to make difficult decisions about whether and when to spend their household resources on drugs. In poor parts of the world, most people are treated in public health facilities and treatment is funded by international donors. HIV/AIDS It is not only the cost of drugs that creates problems of access: poor people may not be able to afford transport to clinics, and since some drugs must be taken with food, the effectiveness of treatment may be diminished if patients are malnourished. Poverty therefore affects adherence to and success of treatment. Tuberculosis and HIV The issue of TB and HIV is not fully understood outside the medical arena. While most diseases that affect HIV-positive people are not a threat to others, TB is an exception. The WHO says that HIV/AIDS and TB are so closely connected the terms ‘co-epidemic’ or ‘dual epidemic’ can be used to describe the relationship, and HIV and TB have variously been referred to as ‘the terrible twins’ and ‘Bonnie and Clyde’. Each disease speeds up progress of the other: TB shortens the survival time of people with HIV/AIDS, killing up to half of all AIDS patients worldwide; HIV-positive people have increased likelihood of acquiring new TB infection, are more likely to develop active TB, and relapse if previously treated. Having HIV makes the diagnosis of TB more complex, and prophylactic and curative treatment for TB in HIV-positive people is more costly and problematic. 34 The WHO recommends that TB patients be offered voluntary counselling and testing for HIV, while people who are HIV infected should be tested for TB and treated or given prophylaxis. Ideally, TB patients should have their disease brought under control before being put on ART. Towards the end of 2006, there were reports from South Africa of an outbreak of extensively drug-resistant (XDR) TB, a form that is extremely difficult to treat as few drugs are effective. In one hospital in Tugela Ferry, of 542 TB patients, 53 had XDR TB, and 52 of these patients died within weeks of being tested. Of the 53 patients, 44 were tested for HIV and all were positive. While this outbreak caught the attention of the media, in March of 2006 the CDC and WHO had already reported XDR TB from 17 countries. The links between TB and HIV have the potential to make HIV a broader public health issue. Exposure to TB is more difficult to control since the bacteria that cause it are airborne. In settings where large numbers of people are HIV positive, a serious TB epidemic may occur with consequent increased illness and death for those infected, as well as increased risks to the broader general 35 How HIV/AIDS works and scientific responses TB infections are spreading at the rate of one person per second. Every year 8–10 million people catch the disease and 2 million die from it. About 2 billion people carry the bacteria that cause TB, but most never develop the active disease; around 10% of infected people actually develop symptoms, although this proportion is rising as the number of people with weakened immune systems grows. Most cases of TB can be treated, and the DOTs regime (Directly Observed Treatment, short course) has dramatically raised cure rates. However, as with HIV, the number of drug-resistant cases is growing, and up to 50 million people worldwide may be infected with drug-resistant TB. Treating multi-drug-resistant (MDR) TB takes up to two years (as opposed to six months for DOTs) and is more complex and expensive. population. This has been largely ignored or skated over by public health professions and the media. There is a growing recognition that TB and HIV programmes need to work together to achieve effective control of the diseases. Furthermore, the outbreak of XDR TB reveals the weaknesses in existing public health and disease control programmes. HIV/AIDS Biomedical interventions: vaccines, microbicides, and circumcision The ultimate scientific solution to HIV would be a cheap, effective vaccine. Since Edward Jenner vaccinated an eight-year-old boy against smallpox in 1796, vaccines have been seen as a way of eliminating diseases in populations. The first disease to be eradicated worldwide was indeed smallpox – the last ‘wild’ case occurring in 1977. Vaccines now provide protection against a range of childhood diseases including measles, mumps, and rubella. Unfortunately progress towards a vaccine for HIV is slow. The International AIDS Vaccine Initiative (IAVI) notes that there are difficult scientific questions impeding development of a vaccine. There are also economic issues: vaccine development is resource-intensive and, although most research is conducted in the rich world, there is little commercial incentive – the market is limited and risks are high. When a vaccine is developed, there will be questions about its efficacy. What level of protection would it offer, and for what duration? Would one inoculation be sufficient, or would boosters be required? There is a danger that a vaccine might give people a false sense of security and increase the spread of HIV because of continued or even increased unsafe sexual activity. A microbicide is a substance (gel or foam) that could be inserted into the vagina prior to intercourse, to kill viruses and bacteria. This would provide women with protection they could control. 36 Development of microbicides has been incomprehensibly slow. Unlike vaccines, the reason is not primarily scientific but to do with the markets and gender inequity – the main market would be poor women in poor countries who have little spending power. Nonetheless, there are currently 60 substances being studied as potential microbicides and five tested for safety, and it is possible that, should safety and efficacy be established, a microbicide could be available by 2012. Early analysis by Australian demographers Jack and Pat Caldwell suggested there were links between male circumcision and patterns of HIV. The science is clear. In uncircumcised men, the area under the foreskin and the foreskin itself contain many of the cells the virus binds to (the Langerhans’ cells), and the skin or mucosal surface of the foreskin is more easily penetrated. Circumcised men are less likely to contract and pass on other sexually transmitted infections. In South Africa, a study at Orange Farm outside Johannesburg suggested circumcision could be 60% protective against HIV infection. The study was stopped in November 2004 after interim analysis showed ‘the protection effect’ of male circumcision was so high that it would have been unethical to continue. Similarly, in December 2006, the US National Institute of Allergy and Infectious Diseases (NIAID) halted two trials of adult male circumcision because data showed medically performed circumcision greatly reduced male risk of HIV infection. In Kisumu, Kenya, there was a 53% reduction of HIV acquisition 37 How HIV/AIDS works and scientific responses Research into vaccines and microbicides is increasingly supported by a number of philanthropists, including the Bill and Melinda Gates Foundation. While this support is welcomed and important, there is a danger of seeing money and science as providing the solutions to the epidemic. Both interventions are some years away, and even when they do become available they will be only part of the solution. in circumcised men, and in Rakai, Uganda, HIV acquisition was reduced by 48%. HIV/AIDS In March 2007, WHO and UNAIDS issued their conclusions and recommendations on male circumcision for HIV prevention. They found that male circumcision, without doubt, reduces female-to-male HIV transmission and should be recognized as an important additional prevention strategy. While access to circumcision should be made available for men and adolescent boys, it is less complicated and risky for infants, and so neonatal circumcision should be promoted. However, circumcision raises similar questions to vaccination – would those who are circumcised behave in a more risky manner because they believe themselves to be protected? There are also gender issues. It is only male circumcision that is protective; there is no evidence to suggest that male circumcision reduces transmission from infected men to uninfected women. Clearly, though, if fewer men are infected then their female partners are also less likely to be infected. At present, the major determinant of circumcision is religion; it could, in the era of AIDS, become a medical rather than solely cultural practice. 38 Chapter 3 The factors that shape different epidemics Epidemic disease, and AIDS in particular, is a disease of the body – but it is the presenting symptom. The manifestations of AIDS, illness and death, reveal the fractures, stresses, and strains in a society. This chapter shows that while at the most proximate level the chance of HIV transmission may depend on biological determinants, there are other factors that need to be considered, in particular social and economic poverty and inequality. The overview of global epidemiology in Chapter 1 showed a range of epidemics. In a few places prevalence has peaked and fallen; in others it has risen to unexpected levels and remains high. There are settings where all the factors that would facilitate HIV spread seem to be in place yet there is no epidemic. While biomedical factors are critical, it is ultimately behaviours that will determine the shape of the epidemic. These depend on social and environmental factors – the position people occupy in society, their economic status, and how they are perceived and value themselves. Where vulnerabilities converge, we see the most serious epidemics. If we can explain existing epidemics, can we predict new ones? Where prevalence has fallen, can we understand what happened in order that it can be replicated elsewhere? 39 HIV/AIDS Infections and epidemics don’t happen randomly. Some diseases are limited to certain geographical environments – for example, to catch malaria a person must be in a malarial area and bitten by a mosquito carrying the parasite. People must be exposed to the pathogen. Even then, for an infection to take hold, the immune system must be unable to resist the disease-causing organism. This is true of all infectious illnesses: we see it every year with the common cold, when most people are exposed to the virus, but some individuals manage to stave off infection while others fall sick. Thus an individual’s immune status is important in determining whether or not they are infected and how severely they are affected. Drivers of disease are mostly social and economic. For example, living in poorly ventilated, crowded rooms increases the risk of exposure to and of contracting TB. Being undernourished and/ or lacking vitamins and micronutrients will increase susceptibility to a plethora of illnesses and means people are sicker for longer. Disease, globally and nationally, flourishes where there is poverty. In the rich countries of the world, the greatest disease burden is found among the poorer populations: those who are ill-nourished, poorly housed, and less well educated. With regard to nations, broadly speaking it is in the poorer ones where disease is more likely to thrive. Critical factors that can mitigate against poverty are social services and public health. Thus Cuba, or Kerala state in India, have healthier populations than their richer more inequitable neighbours. On occasion there is a convergence of vulnerability that results in epidemic outbreaks. For example, prior to 1991, cholera had not been seen in the Americas for 100 years. In that year an outbreak began in Peru, after a ship in Lima harbour pumped its bilges of water that was contaminated by the Vibrio cholerae bacteria. The disease took hold in the city’s slums, and then spread from slum 40 to slum across the Americas. Obviously ships had discharged contaminated water before, both in Lima and other ports. However, in 1991 the slums had grown rapidly, the inhabitants were the victims of a decade of economic crisis which resulted in falling incomes and increased inequality. People were poorly nourished and lacked access to basic infrastructure including water, sanitation, and health services. The result was a regional cholera epidemic. Biomedical drivers The most important biological influences are the virus sub-type and the genetic make-up of those exposed. Some sub-types are believed to be more infectious than others. This may be partly why Southern Africa, where sub-type clade C is found, has such a serious epidemic. The genetics may be important, operating at the individual or population level, making some individuals or groups more or less susceptible. This is controversial, as it is sometimes interpreted as a form of ‘genetic determinism’ instead of the natural ‘reality’ that results from the diversity of humankind. Evolution is not ‘kind’ or ‘cruel’, although we may wish to construe it as such. The importance of the virus type and genetics are areas of continuing scientific research. The stage of infection is crucial. For several months after infection, there is an intense battle between the immune system and the virus. During this period, the semen, vaginal fluids, and blood contain many virus particles, increasing the chance of infection for sexual partners and people who share injecting equipment. There is then a period when the body rallies and the 41 The factors that shape different epidemics In order for a person to become infected, they must be in contact with HIV with sufficient exposure for the infection to take hold. Once contact has occurred, biomedical factors are the key determinant of whether or not a person will be infected. viral load is low. As the infection progresses, it will slowly climb and the CD4 cell count will fall, as shown in Figure 5 of the previous chapter. HIV/AIDS Once the epidemic gains a hold in a society, it has a built-in momentum. The more people with early-stage infection, the greater the chance of someone having sex with such a person and being infected, so that a vicious cycle develops. The virus has to breach the natural defences of the body, the skin or mucous membranes. Risk is higher for women as semen remains in the vagina after unprotected intercourse. This partly accounts for the greater number of women infected in heterosexually driven epidemics. The danger is increased by tearing in the vagina, which may occur during abusive sex or rape, especially in younger women whose vaginas are not mature, and thus interventions that delay sexual debut reduce transmission. Condoms provide a barrier, but are not female-controlled. Sexually transmitted infections (STIs) are an important biological co-factor. Those that cause genital ulcers such as herpes, chancroid, and syphilis create a portal for the virus to enter the body, and at the same time the presence of the cells HIV seeks to infect, CD4 cells and macrophages, is increased. In a person with an STI, the number of virus particles released into blood, semen, and other body fluids increases, even if the infection is asymptomatic. An HIV-infected person is more likely to be infected by STIs and the severity and duration of these infections will be increased. After sexual transmission, the next most important route of HIV infection is mother-to-child transmission (MTCT) with infants exposed through birth or breast-feeding. The viral load of the mother influences the probability of infection of the infant – the higher the load, the higher the risk. However, if a women has 42 advanced disease, the chance of falling pregnant and carrying a child to term is decreased. Other biomedical drivers include the use of unsafe blood and blood products and nosocomial (hospital-acquired) infections. In India in 2001, of the risk/transmission categories listed by the National AIDS Control Organization, 4.1% of AIDS cases resulted from contaminated blood or blood products. The practice there of paying blood donors may result in contaminated blood being collected, paid donors being more likely to live on the margins of society and to be infected. In China, it was estimated in 2002 that 9.7% of HIV cases were transmitted through illegal and unsafe practices associated with blood plasma collection. One under-researched area is the effect of ill health from other causes on HIV transmission. There is evidence to suggest that any other infection will cause the viral load of HIV to rise rapidly and remain high for some time afterwards. For example, research shows that when an HIV-positive person has malaria the amount of virus in the blood increases tenfold, and thus such a person will be more infectious to his or her sexual partners. They may not want to have sex while they are sick, but when they recover their sex drive will return and infectivity is still high. Research in Kisumu in Kenya estimated that 5% of adult HIV infections were linked to malaria, and conversely, HIV 43 The factors that shape different epidemics While ‘nosocomial’ usually means infections acquired in hospital, with regard to HIV/AIDS it is taken to mean all infections transmitted in health care settings. If equipment is not adequately sterilized, then there is a danger of patient-to-patient transmission. Health workers are at risk through accidents involving body fluids such as needle stick injuries. All those caring for AIDS patients, including in the home, face some degree of danger and this rises if carers don’t have adequate protective equipment such as gloves. Sharing drug-injecting equipment is an efficient way of spreading HIV, and this is the main driver in some settings. infection increases susceptibility to other diseases, the Kenyan research also suggesting 10% of malaria cases were due to HIV. An HIV-positive individual with any other infection is likely to be sicker for longer and may be more likely to die. Whether or not a man is circumcised, a biomedical solution, is important, as was discussed in the previous chapter. The routine offering of circumcision for male infants delivered in health care settings makes sense, but will take 20 or more years to impact on HIV prevalence. Had this happened in 1985, we would be reaping the benefits today. HIV/AIDS Behaviours In order for biomedical factors to come into play, a person has to have sex, or share needles with someone who is infected. There are a range of behaviours that increase risk. The AIDS epidemic has taught us unexpected lessons about human sexuality. The frequency of sexual intercourse does not vary greatly from country to country. There are a wide and intriguing variety of sexual practices, most of which are harmless and many are considered ‘normal’. The behaviours that facilitate the spread of HIV are complex and dynamic, but global data suggest it is common for people to have more than one partner in their lifetime. If someone does not have sex or sticks to one uninfected partner, then that person won’t be sexually exposed to HIV (or any other sexually transmitted infection) provided their partner is also faithful. This applies in all sexual relationships – hetero- or homosexual. In societies where polygamy is practised, then as long as all parties are faithful, the same protections apply. Early AIDS prevention posters which, in most countries, said unequivocally ‘Stick To One Partner’ had to be adapted for Swaziland where polyandry is accepted and the king also has many wives – here, the posters had the less than catchy message: ‘Be Faithful in Your Polygamous Family’. 44 Data on sex and sexuality We are all intrigued by sex and sexual behaviours, but collecting this information is complex. The first major study was by Dr Alfred Kinsey of Indiana University. The Kinsey Reports comprise two books on human sexual behaviour: Sexual Behavior in the Human Male (1948) and Sexual Behavior in the Human Female (1953). When released, this research was controversial, not just for the subject matter, but because it challenged many beliefs about sexuality, including the ideas that heterosexuality, faithfulness, and abstinence were ethical and statistical norms. A basic problem with sexual behaviour data is that they are self-reported. This means that the data are subject to bias. 45 The factors that shape different epidemics Key behavioural factors are the age of sexual debut, sexual practices, number of partners, frequency of partner exchange, concurrency of partners, and mixing patterns including intergenerational sex. The younger a woman begins penetrative sex, the greater her risk of infection due to the danger of tearing of the vagina. The age of sexual debut is determined by her behaviour and those of her partners, and is influenced by social norms. Globally, data suggest that females have sex earlier than men, but trends for age at first sex are not clear. A meta-analysis of global sexual behaviour concluded trends towards earlier sexual experience are less pronounced than supposed. In developing countries, sexual activity is happening later, but prevalence of premarital sex increases if marriage is postponed. The data show the median age for first sexual intercourse for males was 16.5 in Kenya, Zambia, Brazil, Peru, and Britain. In the USA, it was 17.3. The oldest was 24.5, in Indonesia. For women, median age at first intercourse was lowest in a number of African countries: 15.5 in Ethiopia, Mozambique, Côte d’Ivoire, and Cameroon; the oldest was 20.5 in Rwanda. In the UK and USA, it was 17.5. Most commonly, men over-report and women under-report partnerships and frequency of intercourse. This was well described in the title of an article on sexuality in Tanzania: Secretive Females or Swaggering Males? The meta-analysis published in The Lancet in 2006 shows how little data there are on sexual behaviour, and even less longitudinal information. One source of data is the Durex Global Sex Survey carried out annually since 1996. In 2005, it looked HIV/AIDS at 41 countries. It is web-based so has huge biases, but gives comparative and longitudinal data. The question of sexual practices receives more salacious press than is deserved, although it is the area about which we know least. As far as HIV is concerned, some potentially harmful practices are widow inheritance, when a woman is ‘inherited’ by her deceased husband’s brother, and the practice of ‘dry sex’, the use of herbs or other agents to dry out the vagina, which some believe increases (the man’s) pleasure during sex, but the range of practices is immense. It is necessary to be open-minded, identify those that increase risk, understand how they do this, and find out what can be done about them. The number of sexual partners per se seems less important. Men in Thailand (where the adult infection rate is 1.4%) and Rio de Janeiro (adult infection rate in Brazil is 0.5%) were more likely to report five or more casual partners in the previous year than men in Tanzania, Kenya, and Lesotho (where adult infection rates were 6.5%, 6.1%, and 23.2 % respectively). Adult prevalence in Zambia is 17%, but the 2005 Zambian Study found that over 97% of married women and 90% of married men indicated they had no non-marital partners in the previous year. The same survey found 26% of non-married people reported one ‘non-regular partner’ but only 4% reported two or three. 46 The factors that shape different epidemics 6. Needle-sharing, a high-risk behaviour People in industrialized countries do not have significantly more or fewer partners in a lifetime, but their tendency is for serial monogamy. This means that they enter relationships which are maintained for months or years. The relationships involve a degree of commitment, and may be legally recognized as marriage or civil union. Serial monogamy traps the virus within a single relationship and so is not high risk for HIV transmission. The danger of infection increases when people have ‘non-regular’ partners or affairs. 47 HIV/AIDS While frequent partner change is hazardous, it is not common anywhere. The greatest risk is concurrency of partnering, when people have more than one partner and the relationships overlap for months or years. Writing in The Lancet in 2004, Halperin and Epstein noted that because infectivity is higher during the weeks and months after infection, concurrent partnering greatly exacerbates the spread of HIV and may be one of the main drivers. When a person in a network of concurrent relationships becomes infected, everyone is at risk. Mathematical models comparing serial monogamy and long-term concurrency showed that, in the latter, HIV transmission would be more rapid and the epidemic ten times greater. Commercial sex, whether heterosexual and homosexual transactions, is potentially risky both for sex workers and their clients. In many settings, in the early years of the epidemic commercial sex workers were ‘core transmitters’. A modelling exercise in Nairobi illustrated this. It assumed that 80% of sex workers were infected and had four clients per day, and 10% of men were infected and had four sexual partners per year. If women sex workers increased their clients’ condom use from 10% to 80%, that was estimated to prevent 10,200 new infections. Increasing condom use among the men to 80% would avert only 88 infections. In Thailand, the early epidemic was spread by sex workers, but the ‘100% condom campaign’, making condom use in brothels mandatory, was effective at bringing HIV spread under control. In Durban, research in the early 1990s found brothel-based sex workers (who used condoms) had negligible HIV infection. Mixing patterns make it possible for an infection to be carried from one part of a country to another, across national borders, or to be introduced into previously closed circles. Here paths for transmission include both sex and drug use. For example, an oil worker who becomes infected in, say, Nigeria can carry the disease to his home country, then to, say, Indonesia in a matter of days. 48 A central Asian drug user can fly to any European capital in hours. With such mixing there is also the danger of re-infection and of new strains being created. Mixing not only takes place across geographic regions but across age groups. Intergenerational sex, usually where men have younger female partners, is common in many societies. In countries where there is a heterosexual epidemic, the pattern is for women in their teens and twenties to have much higher prevalence than their male contemporaries. This is because they are having sex with older infected men, and sometimes this is transactional – for money, food, transport, and school or university fees. The use of condoms is also a ‘behaviour’. Correct, consistent condom use reduces the chances of HIV infection. When condoms 49 The factors that shape different epidemics 7. Warwick Junction in Durban, South Africa: where thousands of street traders serve many more thousands of daily commuters, and where HIV infection is high were used in risky settings – among young people in Europe and the USA, and in brothels in Thailand – they prevented HIV spread or turned the epidemic around, but it is difficult to achieve consistent use other than in commercial and casual sexual encounters, and women may not have the power to insist their partners use condoms. Social, economic, political, and other determinants HIV/AIDS How people behave may determine their risk of infection, but behaviours result from the environment in which people live and operate. This milieu is, in turn, a function of local, national, and international factors; economics, politics, and culture. These are complex and varied and how we view them depends on our own values, backgrounds, and disciplines. The way the epidemic is influenced by these determinants is best illustrated by examples. In Southern Africa, development of the mines and industry required a large workforce. The dominance of capitalism meant wages were tightly controlled. The colonial history and, in South Africa, subsequent apartheid legislation resulted in black labour being most exploited. Apartheid imposed strict controls on where black people could live and work and meant many South Africans were classified as migrants, effectively foreigners in their own country. Huge numbers of men travelled to work in the mines, factories, and on the farms. Foreign migrant miners were drawn primarily from Malawi, Lesotho, Botswana, Swaziland, Mozambique, and Namibia, and in the 1970s there were close to half a million foreigners employed on contracts in South Africa. In 1985 nearly two million black South Africans were classified as migrants. These people lived apart from their families, in hostel accommodation, and had to return home between contracts. The effects of this dislocation and disempowerment have been well documented. When people are placed in circumstances in 50 which they cannot maintain stable relationships, life is risky and pleasures are few and necessarily cheap, then sexually transmitted diseases will be rampant. This was true for all migrants. For migrant miners, their work was particularly dangerous, their control over most aspects of their lives was minimal, and they were disempowered in many respects. However, they had regular incomes. When gender inequality and the extreme poverty in the surrounding communities is considered, an ideal setting had been created for the spread of sexually transmitted infections. Similar stories can be told of former communist countries. The collapse of communism was not good news for millions of citizens of the Soviet Union and Eastern Bloc. The system had provided many benefits, citizens were assured of employment, education, housing, health care, and even holidays; basic needs, and more, were met. The collapse of these economies has also been well documented. In the Ukraine, the per capita GDP (in purchasing power parity) fell from US$ 6,372 in 1990 to a low of US$ 3,194 in 1998. In 1994 alone, GDP declined by 22.9%. From having full employment, by 2000 the number of unemployed had reached close to three million, 12% of the economically active population. The pattern of societal collapse is seen across the region. Alcohol abuse was always common, but intravenous drug use increased dramatically, especially among the dispossessed and lost youth. The epidemic here has been driven by drug use – but this in turn is the result of economic and social disintegration and the 51 The factors that shape different epidemics During the 1980s, four large surveys were carried out to establish if HIV was present in South African populations outside of known high-risk groups. HIV was found by only one survey. The few cases were Malawian miners. Migration to and within South Africa created the perfect environment for the spread of HIV, not only in labour centres but in the migrants’ home communities. The fracturing of families, changing gender dynamics, and increased poverty were major causes of the high levels of HIV. consequent blow to the morale, hopes, and dreams of the younger generation. HIV/AIDS In China, the epidemic of HIV among people selling blood, described in Chapter 1, has its roots in the political economy of the country. The peasants from whom the blood was collected are among the poorest, and selling blood is a survival strategy. The collapse of state medicine and introduction of fees meant that a ready, and unregulated, market existed. Ultimately, embracing the globalized economy will have partly driven China’s epidemic. Gender relations shape risk and behaviours. A woman’s biology puts her at greater risk. Of crucial importance is the lack of power, and violence against women. Girls often feel pressured or forced into having sex. The Reproductive Health Research Unit Survey in South Africa reported that 28% of females and 16% of males aged 15 to 24 either ‘did not want’ or ‘really did not want’ their first sex. In Zambia, the Sexual Behaviour Survey in 2005 found 15.1% of females reported they were forced to have sex, and in 67.5% of cases it was by their husbands/boyfriends. Some customs encourage early marriage and pregnancy; the marriage of young women to older men; and unequal partnering. These accept male dominance and female subservience. Globally, social norms emphasize female chastity and turn a blind eye to male promiscuity. In most of the poorer world, women are economically dependent on men, and sex work is the most extreme manifestation of this. Enabling female control of reproductive health would help the response to HIV/AIDS. The relationship between HIV/AIDS and poverty is complex, both at the individual and national level. Botswana is, by most standards, a wealthy country. With a per capita income of US$ 4,372 in 2003, it has the third highest income in sub-Saharan Africa; Senegal by contrast has an income of just US$ 634 per capita. The prevalence rates among adults aged 15 to 49 in these 52 countries are 24.1% in Botswana and 0.9% in Senegal. It would seem that simply being poor does not determine a country’s HIV prevalence; rather, what is crucial is societal equality. Conclusion While, at the most proximate level, the chance of HIV transmission may depend on biological determinants, they are only a part of the picture. Developing drugs, vaccines, and microbicides, circumcising men, and putting people on treatment are technical and biomedical responses. Unfortunately, this disease does not lend itself to simple technical solutions. The real challenge is to change behaviours to reduce risk. Behaviours can be modified, and the evidence suggests that there are a few key interventions that would have a significant impact on the progress of the epidemic. These include reducing concurrent partnering and delaying sexual debut for young women. Beyond this are the messages that have been used since the early days of the epidemic: abstinence
