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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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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:
John Parker and Richard Rathbone

L. Sandy Maisel

PRESIDENCY Charles O. Jones
Julia Annas

Harry Sidebottom

John Blair

Andrew Ballantyne

ARISTOTLE Jonathan Barnes
ART THEORY Cynthia Freeland

ASTRONOMY Michael Hoskin
ATHEISM Julian Baggini
AUGUSTINE Henry Chadwick
BARTHES Jonathan Culler
BESTSELLERS John Sutherland
THE BIBLE John Riches
THE BRAIN Michael O’Shea
Anthony Wright

BUDDHA Michael Carrithers
BUDDHISM Damien Keown
Damien Keown

CAPITALISM James Fulcher
THE CELTS Barry Cunliffe
CHAOS Leonard Smith
Michael Allingham

Beth Williamson

CLASSICS Mary Beard and
John Henderson

Helen Morales

CLAUSEWITZ Michael Howard
Robert McMahon

Susan Blackmore

Julian Stallabrass

Simon Critchley

Christopher Tyerman

Fred Piper and Sean Murphy

David Hopkins

DARWIN Jonathan Howard
Timothy Lim

DEMOCRACY Bernard Crick
DESIGN John;  Heskett
DINOSAURS David Norman
Patricia Aufderheide

DREAMING J. Allan Hobson
DRUGS Leslie Iversen
THE EARTH Martin Redfern
Partha Dasgupta

Geraldine Pinch

BRITAIN Paul Langford

EMOTION Dylan Evans
EMPIRE Stephen Howe
ENGELS Terrell Carver
ETHICS Simon Blackburn
John Pinder and Simon Usherwood

Brian and Deborah Charlesworth

FASCISM Kevin Passmore
FEMINISM Margaret Walters
Michael Howard

FOSSILS Keith Thomson
FOUCAULT Gary Gutting
William Doyle

FREE WILL Thomas Pink
FREUD Anthony Storr
Malise Ruthven

GALILEO Stillman Drake
Ken Binmore

GANDHI Bhikhu Parekh
Bill McGuire

Manfred Steger

Mark Maslin

Eric Rauchway

James Gordon Finlayson

HEGEL Peter Singer
HEIDEGGER Michael Inwood
HIEROGLYPHS Penelope Wilson
HISTORY John H. Arnold
HIV/AIDS Alan Whiteside
HOBBES Richard Tuck
Bernard Wood

Andrew Clapham

HUME A. J. Ayer
IDEOLOGY Michael Freeden
Sue Hamilton

MIGRATION Khalid Koser
RELATIONS Paul Wilkinson
ISLAM Malise Ruthven
JOURNALISM Ian Hargreaves
JUDAISM Norman Solomon
JUNG Anthony Stevens
KAFKA Ritchie Robertson
KANT Roger Scruton
KIERKEGAARD Patrick Gardiner
THE KORAN Michael Cook
LINGUISTICS Peter Matthews
Jonathan Culler

LOCKE John Dunn
LOGIC Graham Priest

MACHIAVELLI Quentin Skinner
John Phillips

MARX Peter Singer
Timothy Gowers

John Gillingham and
Ralph A. Griffiths

MODERN ART David Cottington
Senia Pašeta

MUSIC Nicholas Cook
MYTH Robert A. Segal
NEWTON Robert Iliffe
NIETZSCHE Michael Tanner
Christopher Harvie
and H. C. G. Matthew

Marc Mulholland

PAUL E. P. Sanders
Raymond Wacks

Samir Okasha

PLATO Julia Annas

POLITICS Kenneth Minogue
David Miller

Robert Young

Christopher Butler

Catherine Belsey

Catherine Osborne

Gillian Butler and Freda McManus

John Polkinghorne

RACISM Ali Rattansi
Jerry Brotton

Geraldine A. Johnson

Christopher Kelly

ROUSSEAU Robert Wokler
RUSSELL A. C. Grayling
Catriona Kelly

S. A. Smith

Chris Frith and Eve Johnstone

Christopher Janaway

SHAKESPEARE Germaine Greer
SIKHISM Eleanor Nesbitt
John Monaghan and Peter Just

SOCIALISM Michael Newman
SOCRATES C. C. W. Taylor
Helen Graham

SPINOZA Roger Scruton
Charles Townshend

THEOLOGY David F. Ford
Leofranc Holford-Strevens

TRAGEDY Adrian Poole
BRITAIN Kenneth O. Morgan
THE VIKINGS Julian Richards
WORLD MUSIC Philip Bohlman
Amrita Narlikar

Available soon:
1066 George Garnett


Katerina Reed-Tsocha

GALAXIES John Gribbin
GEOGRAPHY John Matthews and
David Herbert

Nicholas Boyle

Elleke Boehmer

Joseph M. Siracusa

QUAKERISM Pink Dandelion
Thomas Dixon

William Bynum

MEMORY Jonathan Foster

SEXUALITY Véronique Mottier
Terry Eagleton

For more information visit our website

Alan Whiteside

A Very Short Introduction



Great Clarendon Street, Oxford OX2 6DP
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Oxford is a registered trade mark of Oxford University Press
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 Alan Whiteside 2008
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First published as a Very Short Introduction 2008
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without the prior permission in writing of Oxford University Press,
or as expressly permitted by law, or under terms agreed with the appropriate
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and you must impose the same condition on any acquirer
British Library Cataloguing in Publication Data
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Library of Congress Cataloging in Publication Data
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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


Preface xi
Abbreviations xv
List of illustrations xvii
List of tables xix


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


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
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



acquired immunodeficiency syndrome
antenatal clinic
antiretroviral therapies
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


Treatment Action Campaign
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


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.


Viral load and CD4 cell counts
over time 27

6 Needle-sharing 47
© Ed Kashi/Corbis


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

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

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

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,


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.


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

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

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

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


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








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.

The emergence and state of the HIV/AIDS epidemic



The global and regional epidemics


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

Table 1. Regional HIV and AIDS statistics, 2003 and 2005


(15+) and
Adults (15+) children
and children newly
living with
with HIV


and child
deaths due

Sub-Saharan Africa
24.5 million

2.7 million


2.0 million


23.5 million

2.6 million


1.9 million

North Africa and Middle East

440 000

64 000


37 000


380 000

54 000


34 000


8.3 million

930 000


600 000


7.6 million

860 000


500 000


78 000

7 200


3 400


66 000

9 000


2 300

140 000


59 000

Latin America

1.6 million


The emergence and state of the HIV/AIDS epidemic


Table 1. (Continued)


(15+) and
Adults (15+) children
and children newly
living with
with HIV


and child
deaths due


1.4 million

130 000


51 000


330 000

37 000


27 000


310 000

34 000


28 000


Eastern Europe and Central Asia

1.5 million

220 000


53 000


1.1 million

160 000


28 000

North America, Western and Central Europe

2.0 million

65 000


30 000


1.8 million

65 000


30 000


38.6 million

4.1 million


2.8 million


36.2 million

3.9 million


2.6 million


HIV antenatal prevalence in southern African countries

Percentatge prevalence




South Africa



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

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


The emergence and state of the HIV/AIDS epidemic



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.


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


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


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

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

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%.


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


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


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




Incidence rate
per 1000


9 750



10 000




10 250



10 500


Deaths of
Prevalence infected
rate (%)


Year zero






Slow increase






10 750







11 000







11 250







11 400







11 400







11 300






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
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


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.


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

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







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


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.


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
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%.

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


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


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

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.

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.


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


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
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


How HIV/AIDS works and scientific responses

4. The HIV life cycle

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


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

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


Clinical Latency


0 3 6 9 12



3 4 5 6 7 8

5. Viral load and CD4 cell counts over time

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.


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.

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

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.

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.

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


0 to 6:100


Parenteral transmission
Transfusion of infected blood




Needle stick


Needle stick/AZT PEP


Transmission from mother to infant
Without AZT treatment


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

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

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.


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:


‘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.


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.


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


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


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.


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
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
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.

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

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%.


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.


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?



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


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


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.


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
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

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

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.


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’.

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.


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


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.

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.



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.

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

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


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
The effects of this dislocation and disempowerment have been
well documented. When people are placed in circumstances in

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

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


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

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.

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