The African AIDS epidemic: a history

111 Pages·2006·34.92 MB·English

by  John Iliffe

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Flrst published 200!)
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TSBN 13: 9'7R-08S2'1S-WJ0-4 {James Cnrrt.'Y pap~1i 3 Epidemic
ISH'I 13: g78-0~82J4~J 688-4 (Ohio llniversity Press cloth) in Western Equatorial
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British Library Cataloging in PnhHcatinn Data The Conquesi
lliffe. john
T(w African Aid~ epidemic : n hls1ory of the South 33
L Aid~ (Disease) /\Jrica Epidemks - Africa Hi~<to:-)
20th ceuiury i. Epidemics- Africa- Hb!Pry- 21st Century
T. Tille 6 The Penetration
fi !4. )'99 l'!2"(1(J96 of the West
48
tibrarJ of Congress ('ata!oging-in-Pnh~ieation na~a
Wffe, fnhn 7 Causation:
Thf' /\Jrican Aids C'piJ('mic : ft history / John llilTe. A
p. em. 58
Incl1Tdes bibHogrnpbicalleferences m1d index.
!SBN O~R214~ l6RX~X (aile paper) ~·ISBN ll~B214~ 16~9 R (pbk : alk. P"Pcr I 8 Responses
1. /\h1s (Dist'ase)--1\t'rica-.-}Jistory. I. Title.
RAh43.R6.A 1SH3 200o from Above
65
TJpesct. in l 0/10. S p1 Ptwtlrw by Long House, Cmnt1ria 9 Views
Prinl·ecl <md honnd in Britilin at the UnivPrsity F're~:->, Cambridge from Below
80
v
vi Contents
]0 NGOs
& the Evolution of Care 98
De at l! 11reface
8r the Household 1 I
The EpidPmic Matures
1
Conlainrnent
14 'J[-
Conclusion am indebted to the staiT of many libraries: University Li_hrary, i\iedical
Librm y. Afriran Stndies Centre Library, and St John's College Library,
_ __ Cambridge; London School of Hygiene and Tropical Medicine: School of
Oriental and African Studies. London: British Library for Development Studies.
Notes
Falmer: British Library. London and Boston Spa; Library of Congress, \Vash-
202 ington: South African National Library. Pretoria ;:md Cape Town: University of
Further Reading
Cape Town Library: Cullen Library, University of the VVitwatersrand: Ministry
r>f Health, Entebbe: Makerere l'nlversity Library: Albert Cook Memorial
Index
Library_ Medical Lihrary, Kenya!ta National Hospit<ll- Nairobi: and
Medical Library, Muhimbili 1\!edical Centre, Dar es Sa!aanL
Among individuals l am especially graicful to Shane Doyle, Pietcr Fourie.
john Lonsdale. Margie Struthers. David Throup, and Megan Vaug!um_ James
Cnrre~' Publishers deserve my thanks for the urgency with which they have
ander!aken
'Writing the hook bas left me with profoand respect for the epidemiolPgists
and medical scientists nn whose work it draws. Jf. through ignorance or
hubris. l lm1·c misrepresented any rJf their findings. 1 apologis~ in advGnce.
John lli!fe
1:Vcsil'm Equotorhrl ilftica
20
2
Soutlrem 1/i'ica
1
sn
4
vii
"1bbrcviations iJ
NS Nevv series
OCEAC
Organisation de Coordination pour !a Lultc contrc les
Endemics en Centrale
PEP FAR
flbbreviaUons Presidential Emergency Programme for Ai.ls Relief
PHC Primary health care
PLWA People living vvilh Aids
l'LWB/\ People living with HfV/ Aids
HNA Ribonucleic acid
SiL\1) South ilfrican
SS,\1 Social Science and
STD
lnmsmilled disease
STJ transmitted infection
S\VAA
Society for Women and Aids in Ah-ica
TAC Treatment ,\ctirm Campaign
iii\!\ £lids clnalusis A/rim TASO The Aids Support Organisation
TIIET;\
Aids i\.cquired innnune deticiency syndrorne Traditional He;1lers and Therapies Against Aids
i\NC African National Congress (of South Africa) TRST1\1H TransucUons of Ih e Royal Society ol Tropical A'/edicine and
iiRHR :lids Research and Hzmum Rctrol'imses 1/uyielle
ART Antirctroviral treatment liMOH Ugcmda of lleahh
ARV Antiretroviral U~BlllS Joirn llnited Nations Programme on Aids
liNDP
AT ICC /\ids training, lnfurrnatkH1 and cnunscihng centre United Nations Development Programme
LING ASS
AZT Azidothymidine United Nations General Assembly Special Session
BI'viJ British ,~1edicalfom nnl TJN!CEF United Nations Children's Fnnd
DNII:UN
C;\R Central African Republic United Nations lntegraled Kegional lnl(mnaiiun Netwurk
LJSAill
CHEP Copperbelt Health Education Project United States Aid i(Jr International llerclopmenr
!JWESO
CRF Circulating recombinant form llgunda Womeu's Emwt to Save Orphans
VCT
DNA Deoxiribonucleic acid Counselling and Testing
IVAMATi\
EJliD Etlliopimz Joumal of Hcait!z Dcve/opnzwt People Struggling Against Aids in Tanzania
FACT Family Aids Caring Trust WlJO VVorld Healtlz Organisation
\VHO:GPA
Fi\0 Food and Agriculture Organbation World Health Organisation: Clobal Programme on Aids
IIAART Highly active anliretroviral therapy
IHV Human immunodeficiency virus
HSV Herpes simplex virus
lTfH llcalth Tmnsiiion Review
IDS Institute of Development Studies
lDU Injecting drug u:;cr , _
lFORD Instilut de Fonn<ltion et de Hcchc;n:he llemugrapluques
/fSii lntcnwUonal Journal uf S'l1)s ami Aids
jA!\1Jl journal of the A mer icnn Ivledicai , \ssociaUon
l\fRC Medical Research Council
JVlONGOs My Own NGOs _
NACOSA National Aids Convention of South A!rica
NACWOLA National Community of vVomen Living wilh i\ids
NAPWA National Association uf People wilh t\iJs
NE]M New Ennland ]oumal of Medicine
NWJ Non-govermnental Oi'ganisaiion
viii
1
Intentions
T
his book has a modest purpos.e. Man. y history students int·erested in
Africa wish to study the HIV /Aids epidemic but are hampered by the
lack of an introduction to the detailed literature. This book is intended
as an introduction, for students and other readers.
The book is not a work of research. A thorough history of the epidemic
during its first thirty years would demand fieldwork in affected communities,
interviews with those involved, and study of unpublished records of inter-.
national organisations, national governments, and private individuals. I have
not attempted any of these, nor have I the necessary medical and anthro-
pological skills. Instead, the book is a synthesis of the more important and
accessihlt> published material, put into a historical form.
A Ju,l.urical account offers four advantages. First, it suggests an answer to
the question posed most provocatively by President Mbeki of South Africa:
why has Africa had a uniquely terrible HIV I Aids epidemic?' Mbeki attributed
this to poverty and exploitation. Some earlier analysts suggested that Africa
had a distinctive sexual system.2 This book, by contrast, stresses historical
sequence: that Africa had the worst epidemic because it had the first epidemic
established in the general population before anyone knew the disease existed.
Other factors contributed, including poverty and gender relationships, but the
fundamental answer to Mbeki's question was time. Like industrial revolutions
or nationalist movements, Aids epidemics make sense only as a sequence.
Second, a historical approach highlights the evolution and role of the virus.
Because HIV evolves with extraordinary speed and complexity, and because
that evolution has taken place under the eyes of modern medical science, it is
possible to write a history of the virus itself in a way that is probably unique
among human epidemic diseases. At the same time, the distinctive character
of the virus - mildly infectious, slow-acting, ineradicable, fatal - has shaped
both the disease and human responses to it.
Third, many aspects of the epidemic come into focus only when seen in the
longer context of African history. Although HIV/Aids was profoundly different
from earlier African epidemics, it arose from the human penetration of the
natural ecosystem that is the most continuous theme of the African past. That
2 Illtentions
21
tbe virus created a continental epidemic, however, was a consequence of
Africa's massive demographic growth, urbanisation. and social change during
the later twentieth century. Everywhere the took its shape from lbe
structure of the commercial economy lhal had grown up during the colonial
()rig ins
Human responses, in turn, became p;:,ri of <tn tlngoing interaction
between inherited moral understandings of disease and the medical explana-
tions propounded by international authorities and modern i\ldcan doctors.
Like all great epidemics, HIV/Aids became a cataJY',L of ch<Jnge, but in
directions already set by longer historical processes.
Finally, the African epidemic has itself changed over time. H is still at an
early stage: 'the end of t!Je beginning', as the head of the LJNAillS orgunisaiion
described it in 2001.3 Yet in much of AJrica the epidemic bas already evolved
[rum explosive expansion to maturity, while human responses have graduated
from unwilling vulnerability lo planned containment. Tn the proc:ess, mauy 'l.r·lhe
Africans have displayed the endurance common throughout their history.
earliest cunvincing evidence !lf ll10 human irnmmwctdkien,:y virus
Their experience has taught the world muc!J of what it knows about HIV/Aids.
(H!V) thai causes !be acljmred immune ddicicncy syndrome (Ahls) was
Tt is lime tel give that experience a hisiOncal shape. gcilhercd in 1959 amidst the collapse of European colonial rule in
Afrka. ln !cmuary l 959 rioters briefly seized Ctm!rol of the f\li·ican !ownships
of Leopoldville, lhe capital of lhc Bc!gi<m C.mgo, siwcb.ing ils rulers into frantic
decokmbaliou. ln the same year an Arneri.can researcher swdying malaria
toDk blood specimens from patients in Lhe c:ily. When testing procedures !(Jr
HJV became available during the mid 198Us, 671 of his 1\·ozcn specirnetls hum
or
diflenmt parts CljtHil<ll'i<tl Africa lVere le~,tt;tL one proved posilive. [t
came from an urmamed African mall in Lcupuldvili", now ren<Hlled Kinshasa.
The lest was confirmed by the Western R),ll technique - generally considered
lhe most re!i<Jble method - and by dilkrent procedures ill three other
laborawrics1 Although nothing of this kind cc.n be absolutely certain, there
un' strung grounds to believe that IHV existed at Kinshasa in 1959 and that
it \Vas ran~.
One impul'lancc of the Kinohasu case is to establish a date by which lilV
existed. but in itself J;hc case docs not imply that the i\ids epidemic began in
western equatorial ;\Ji·inL lf that unnamed African h;;t! bcc~n the llrst person
e\·er infcdet! with HlV. il wrmld have heen an incredible coincidence. Once
Aids was recogl!lscd as a medicul c·ondiiiun cady in the 1980s, researchers
fuund several early accounts of patients whose recorded symptoms bad
rt'~'embled iL2 Ln~: i\Inntagnier, whose laboratury first iden!i11cd ll!V, thonghl
llwt the earliest case had been aH American man who dic;d in 1952 allcr
s1 d1cring [c\'er, mah1ise. ant! especially tl1e )Jili'WilOC!JSLis carinii pnetrmonia that
alliictcd larer i\mericun Aids patiems,' but no blood bud been :,tnred f(x later
testing and the symptoms demonstrcaed lllliy suppressiou of tile immune
~ystem, fur '.vhkh there could have bceu rec1;,uns other than lH\'. Tlw smnc
was lrue of a Japanese Canadian who died in 1958 e~ud a llalli<lll :\mericun
iu 1959. More cunvincing was the cuse of a liJieen-year-olu, sexually active
American youth who died in 1 'Jb'J with multiple symptoms illduding an
: ::ssive form of Kapusi's sarcoma, a mmour common in later £\ids patients.
!Ji:, :;wred hloud tested ptJSilive for HlV by Wesicm B!rJt, but the was
4 Oliyins
Oriuins 5
!aler questioned. Other possible early cases were found in wcslem luving infected the 1\lorwegian seaman during ihe l960s, but it remained
Africa. There was no stored blood by which to cunfirm a specialist'::; retro· brgely cnn[ined to the Yicinity of Camemnn, even there causing !ewer !iwn
spcciive diagnosis of Aids in an :\frican woman who was hospitalised a! Lisala l () per c,;nll of HlV caoes ill the early 2U00s. l;roup N was a Idler
on !he middle Congo in ] 958 and died in Kinshasa four years later aflc'r trilnsrni~sion auJ retnained \'ecy n::~re; in 2U05 on!y seven cases v\rere knovvn,
suffering wasting and Kaposi's sarcoma. But a Norwegian seaman cuntracrtd all in Camaoun."
HIV some time l;ei(Jrc 1966, possibly while vi::;i!ing DiluuJa on ihe coast of Th,; fact that the likely viral ancestor of IHV--1 has b,;eu li•tmd ollly in the
Cameroun in l'Hil-·2. and later infected his wif,· and child; all thre(c relro- chimpanzees of equatorial Albea is nne of the three reasons for
spectively tested IJ!V -positive, altiwugh with a form of the virus diiT,·: · ·.' from thinking that the originated there. The second reason is llmt only that
that found in Kinshasa iu 1959. region harhonr,;d not only all three groups ul IHV-1 but all the subgroups of
These cases are intriguing and were the bases for early controversy about !!,,, dominant group M9 The significance of this point cirises from the nature
the origins of HIV, but they r.cveal li!tk except that it exis!ed bm w<>s rare in of !be vims-'0 The human immunodellciency virus is ulmost incunceivably
the l ':l50s. The real grounds for believing that llle dominant form of the virus smalt one len-thousandth of a millimetre in diameter. ll cnusisls of a
originated in western equatorial 1\ii:ica, probably in the Lroatl area of of genetic information (a genomej surrounded by a protein envelope, the
Cameroun and the Democratic Republic of Congo (DH Congo). lie in three whole ,·unluining nine genes, when:as a human being has 30,000 -40,000.
other directions. One is that HIV clearly results fwm the transmission lo Like aH viruses. H!V hess no liL: of its own but i;, a parasite ur cells,
human beings of the ancient and related simian immunodeflciency \·irus ils Iii(; J\·om theirs. Transmit!ed from one body to another by Llood, gcnil<ll
an infection of African monkeys that had also spread to chimpanzees." Thal t1uids, or human milk, !he virus becomes at! ached lo cc:rlain types of cells, the
such an animal disea~e should pass to humans is not surprising, because most impurtunt being the C!H helper T-cells thal ac!ivate the body's immune
several major human infectious diseases are contracted from animals. notably system. The virus enters a cell and integrates its genetic inl(mllation into ils
plagHe, sleeping sickness, yellow fever, some forms of influenza, and, mosl lwst's, using the ce!i's lile to reproduce itsdf, which b illl: sol,: functiun <lf a
recently. Creutzfeldt-!akob', Disease5 How such a ln1llsmi:;sion tonk place wilh virus. Tn dc.ing so the virus d.:'s!roys lhe hosi cell·· and hence u!tim<Jiely the
HIV will never be knmvn, bul one possibHi1y may have been infection by blood inlntune s:r~lern \/\Thile producing an inHnr.~nse nnrnbcr uf ra:vv virnses to
in the course of hunting as men penetrated the eyunlorial forest. One study of altack further celis. The ptoc:ess lhnn entry intd a cell to !be produclion of new
] .OY9 people engaged in hunting and butchering in Cameroun, published in viruses Lakes on average about two so that HIV passes some
2004, found t:cn who had contracted simian viruses. although in this case not l NO generations a year. Lvforeovcr, lhe reprodl!c!iun proct~ss is prune to error,
HJV.b Aids is a by-product of the human mastering of tbc natural cm·inmn1ent diSC lHV's geuctic informatiou is in the form of RNA (rlbunucldc acid) dud
that has been the: core of A.frican bistory. lllllSt be convc:rted into the DNA (deoxiribonncleic acid) composiug the cell's
SIV has been transmitted from ;:mimals w luumms at lca~t eleven times ;mel g~ncnne. The combination uf speed and error iu nc:produc!ion meaus that HI V
probably many more. There are two forms of the human disease: HI\' ·l, mul<Jtcs at about l per cent per year, or a million time:, li1Her thun is normal
which is responsible fur the glob<.ll /\ids epidemic, and BlV-.2., wbich is less in evolulion.;'
virulent <md infectious and virtually confined lo the West African coast One consequence of this rapid mutation was that \\'hen the M group of
between Senegal and Cote d'lvuire. HIV-.2., discussed in Chapter 6, is closely HJV-1 was the l '!80s awl 1 ')90s, i! displayed great
rciated to the SIV common in the sooty wangabey monkeys uf that region. Using a range of spedmens from All·ica, Nnrtlt America, and Eumpe,
Bv 2005, HlV-2 infections had been divided into eighl groups. each believed resecm::lwrs idernilied ten subgroups that diJTcred from oue another in their
t,;
have resulted from a separate transmission. On1y two nf these groups, composiUuu by up to 30 per cent. They were lettered A, B, C, D, Fl, F2, G, H,
lettered A and B, had established themselves as human epidemks, suggesting J, and KY ;\1! subgroups were f,mnd only ill western cqtmtorial Albea,
thai many unsuccessfltl transmissions may abo have taken place in !he pasL7 alilwugh ii may be more accurate w say that !he lhllesl rang,e of diversity
Ily contrast, the anima[ virus most similar to (alihougb still quite distant c:xiskd only there, heeanse the viruses identified ln the DK C'omw, in
r;~om) IHV-1 and probably ancestral toil is the SIV occa,iunally harboured p<ll'ticulur. show as much diversity within supposed subgn1llps as b;~wcecn
by a species of chimpanzee (Pan troglodytes troglodytes) whos<o natural territory them. This suggests that lHV group ~d evolved and di'\'ersilied in thee broad
is the !~xest of Gabon, Equatorial Cninea, CentrJI African Hepublic, Congo region before certain strains wl:rc carried elsewhere to ,;reate
Cameroun, and Congo-Brazzaville, somewhat nortb of Kinshasa. Three JilTerenliated subgroups by what is called a limnder diec1.1' At all events,
groups of IIIV-1 have been identified and lettered 1\I, N, and 0. Each group there is a fund<unental distinction between the greal diversi!y of strains in
must result from a separate transmission of SIV, becanse on a family tree of western CcJUal:orial Alfica and the domim1tion or one ur two subgroups
tbc virus they are separated by intervening SIV :,trains. Gmup M is (sometimes in combination) in every other region of lhe world: A and D in
for the global epidemic that 200S had infected about 60 eastern Africa; a combinatiun of A and c; in West :\frica: B in Europe am!
million people. Group 0 is eqmdiy virulent and may be al !east cqua!ly old, i''urlh 1\merica; C in southern Ai\-ica, Ethiopia, aud lndiaH
fl Orif)ins
Ori[!ins 7
Unlike many olher viruses, such as inllucnza, HlV stnlins do not u'""''''~'" especially successful. By .WO 5, 16 had beeu clussilied as recombi-
one another at intervals bnt evolve and differentiate as !hey pass from one
mmt limns (CRFs), for each uf which al leas! three distinct specimens had been
human hody to £UlOI her. Modern medical science can distinguish in great analysed. The most successful were CEFOJ i\E, the dominam l(>rrn of IllV in
dd.ail between these strains and reconstruct their genetic relationships. This
Asia, and responsible for at least two-thinb of West
makes it possible to write a history of HlV and its epidemic dispersal in a way Ali·ican fHV infectim1s.1'' Recombination is probably at ieast <JS important as
that may be impossible for any other disease, using eviderrce from stored blood
: .. _. iun _i11 accelerating the evolution of I-! IV, but irs implications for dating
and living bodies. The first pari. or this book outlines such a history fur the ba,cd on a-!nokcular clo..:k Me complex and obscure. By blurring dill"ercnces
African continent. Moreover, medical science holds out at least the between subgroups it might mai.:.c evolutionary ever:ls seem more recent than
of dating this history. lt is plausible to argue that 1!1 V mutates so extensively they were. but by tlie number of strains it might make the
that its overall mutation is at a regular speed, wbich can be calculated from events seem more ancient than !hey were. The two IL:ams who estimated dates
the evolutionary distance between classilied specimens taken at known dales. for the diilcrellliation or the l\I group tried to exclude the effects of
This 'molecular clock' can then suggest dates for major evenls iu lhe recornbination, but geneticists feared that the problem was more di!licult and
sequence, such as the separation of one subgroup from another. that ,:onclusions based on a molecular clock 'may he of very limited value'. 20
One such calculation lhJm 144 dated specimens was published in 2000, using I-:!o\VC\Ter uncertain their findings, at1crnpts to dntc the epidetnic daritied
massive computing capacity at Los Alamos. lt suggested !hal the last common several prublems in Together with the identification of the t9 59
ancestor of HIV-l group M- the point a! which the subgroups of lhe global case in Kinshasa. ruled out the theory, propounded in Edward
epidemic began to differentiate - lay <Jrmmd the year 1931, and 1Nith more Hooper's book, The River. thut. 1he IJIV-l t~pidemic had been caused
confidence between 1915 and 1 941. Since tbe researchers knew that the by a polio immnnisation campaigu in the Congo region during 1')57-60 that
genes composing thLo HIV genome mntate at different speeds, they compared allegedly used a vaccine bred on SlY-infected chimpanzee kidneys- a theory
lhis calculation, based on the rnost mutable envelope gene. with a cakulation also conlradicted by negative tests on surviving vaccine samples. Instead,
from a less mlltuble gene, which suggested a 19 34 date. The rc::searcher~ attempts at stimulated interest in the interw<tr period 1.vhen 1he
checked their procedure lbrthcr by independently dating the e<H'iiest HlV diversifkation or group M supposedly began. t~oling that the earliest known
specimen !aken at Kinshasa in 195':!, which had been identilled as an early BTV cases in Afi'ie<1 all occurred in lerrllories, researchers
version of the D subgroup shortly after its separation ll·om the B subgroup. The highlighted colonial innovations there that might have converted occasional
computer dated it bet\l!e~n J 957 and l960Y In 20lll another researcll learn viral transmissions into a dise<h>c capable of epidemic expansion: penetration
published similar calculations based on diflercnt specimens; they dated tbe lao! or 1h e klresL fur rubber coJlection,. and increased viral
common ancestor of group M to 193 7 (by the envelope gene) or ·1 ':!20 the transmission through labour concentrations and vaccine campaigns against
least mutable gene). The second research team also suggested that HIV-1 group sleeping sickness and m1allpox: and the adaptation of the virus to humans
M separated trom the strain of SIV ancestral to ibat in modern chimpanzees lhrough rapid pussaging by arm to-ann inoculation that would have the effect
around 1675, or with more confidence between 15':!0 and 1761.16 It would be of acceleraring evolutim1n No direct evidence linking these innovations to HJV
unwise at this stage to attach too mnch importance to this date. had been published 2005, bnt the problem of how a simian virus might
Among the many uncertainties surrounding these findings, the most become capable of causing a human epidemic attracted the attention o[ olh,,r
relevant here is whether the notion of a molecular clock is invalidated by researchers. HIV-1 group N and at least six transmissions of HIV-2 had not
another feature of viral evolution known as recombination. A person can be become suflkiently !nmsmissabte or infectious as to cause epidemics. These
infected by more than one strain of II!V. If thal occurs, viruses of di!Ierent wccre the limns of Hl\1 most similar to SlV, so il appeared that the mere
subgroups may enter 1.he same cell and, in the process of integrating their transmission of SIV to humans was unlikely to cause w;,!e_:spread disease; the
genetic material with the host's, may prodnce a new strain of virus combining virus must have evolved li:om STV to HJV within human bodies, and it must
elements from two or more subgroups. (SIV is subject to the same process and have done so for the first time and perhaps more or less simultancouslv in two
ibe original simian virus transmitted to humans as the ancestor of FliV-1 groups of HIV-l and two of IHV-2. Preston Marx and olbers argued 'ihat the
group !VI is itself believed to have been a recombinant f(mn.)17 /\II bough the chance of I his happening natttrally was small'. lnstcad, rejecting
slrain identified in 19 59 appears not to have been a recombinant, one of the the 19 j' d".le li.>r the divcrsillcation of ihe l'vl group but accepting 1959 as
earliest recovered from the DR Congo in l 'l76 was, and it is even possible thut the first documemcd HIV case, they ~uggcsted !hat SlV had been converted
supposedly discrete subgroups were products of recombination at a stage so into HIV by rapid passaging through .Mrican populations the 1 ')'ills,
early as to be no longer identifiable. '8 Recombinants can combine with other owing to the introduction of supposedly disposable (but oilen in praciice
recombinants, creating immense genetic heterogeneity, especially in the re-used) syringes to inject penicillin and other new medications. Between
western equatorial region where the epidemic is oldest and the divcr~;ity of l '!52 and !960 ammal world output of syringes increased lhml K million to
subgroups is greatest Certain recombinant forms, however, bave been l ,000 million23
8 Origins
Origins 9
These theories remained theories, but they indicated the kinds of evolu-
not kill but destroys the immune system's capacity to resist other opportunistic
tionary stages that may have produced HIV: probably multiple transmissions
inJections that are ultimately fatal. Some of these, notably ttiberculosis, were
of SIV from sooty mangabey monkeys in West Afi:ica over a long period;
infections already current in the region concerned, so that it may not have
perhaps less frequent transmissions of the rarer chimpanzee virus in western
been easy to discern that a new disease was present. Retrospectively, however,
equatorial Africa; its evolution into HIV within human bodies, whether over
these opportunistic infections are the signs that first reveal the emerging HIV
some centuries or through the unintended effects of medical interventions; and
epide~. Their appearance in western equatorial Africa during the 19 70s is
its emergence by 1959 as a virus capable of causing a global human epidemic.
the third' reason - alongside the location of the simian ancestor and maximum
Yet a difficulty remained: there was no visible epidemic in 1 9 59, nor for
diversity of subgroups - to believe that the HIV epidemic originated there.
another twenty years. The likely reasons lay in three characteristics of the
virus. First, as viruses go, HIV is difficult to transmit. Whereas influenza - 'the
sickness of the air', as it was called in Ethiopia in 1918-can be transmitted
aerially to anyone close enough to inhale it, HIV can be contracted only by
absorption of blood, genital fluids, or milk from an infected human body. In
heterosexual intercourse - the chief means of transmission in Africa - the
chance of infection in one sexual act between otherwise healthy partners has
been variously estimated at between 1 in 10,000 and 1 in 500.24 To create
and sustain an epidemic, therefore, requires special circumstances, but the
chance of transmission increases substantially if either partner has a sexually
transmitted disease or if the already-infected partner is in a particularly
infectious condition. This is the case shortly after infection, when a person is
perhaps eight or ten times more infectious than usual, and in the last stages
of the disease, when infectivity is even greater.25
The difficulty of transmitting HIV relates to the second likely reason for the
slow emergence of a visible epidemic, which was the very gradual develop-
ment of the disease within human bodies. For a few weeks after infection the
virus has the advantage of surprise: viral load rises rapidly, lasting damage
may be done to the immune system, and there may be feverish symptoms,
perhaps often mistaken for malaria. Thereafter the immune system
counter-attacks and an evenly matched war of attrition takes place in which
HIV produces up to 10 billion new viral particles and destroys up to 2 billion
CD4 helper T-cells each day. In HIV-1 this incubation period varies
considerably but may last in adults for an average of nine or ten years - the
period measured by a careful study in Uganda - before the immune system is
so weakened that Aids supervenes. Death in untreated patients then follows
almost invariably and relatively quickly, in an average of perhaps nine or ten
months.26 The infected person remains infectious throughout the disease. This
long incubation period with only sporadic symptoms distinguishes HIV I Aids
from previous epidemic diseases, renders it especially dangerous to human life,
makes it difficult to check, ensures that it does not burn itself out, and, as will
be seen, has given the Aids epidemic its unique character. As a comparison,
the incubation period of influenza is not nine years but one to three days,
while that of plague in Britain, considered unusually long and tL:refore
dangerous, may have averaged about 30 days.27 'What is serious,' a West
African villager said of HIV, 'is that this disease is silent, hypocritical, visible
only when the damage is already irreparable. '28
There was a third reason why the potentially epidemic virus that existed in
19 59 did not breed a visible epidemic for another twenty years. HIV I Aids does
Epid,;Jnic in H'tslrm 1\qu,Jtoria! 1\jrica 11
3
Epidenzic
in Western Equatorial f~/]~ica
f-I
fV-l !lrst became epidemic dnring ihe 1970s in western equahJriol
Africa. its place of origin. H was al llrst a silent epidemic. unnoticed
until established tou firmly to be :,tuppccl. In lhis region, also. during
the mid 1980s. the epidemiology of heterosexual was ilrst dder-
mined. exposing a pattern whose main features were to extend throughoul
sub-Saharan Africa but whose local peculiarities were also to limit epidemic
growth within the western equatorial region itself. From Ibis region. more-
over, variants of the virus were carried to the rest or the continent.
Ahbough HTV-1 had almost certainly existed in H!estcrn eqnalorJ<:Ji Africa
since at least the 1950s, it had hitherto struggled even !o survire in a sparsely
populated region of diflicnlt. often forested environments and poor
communications. This was clear from a group of villages a! Yambuku in the
north of the DR Congo. Blood taken li.·om 659 villagers there in 1976. during
one of tbe first outbreaks of Ebola virus. later revealed !hat five (fUl per cent)
were infecled with HIV. When the villagers were tested again ten years later,
HIV prevalence was still 0.8 per cent. Of blood samples cullec!ed across the
border in southern Sudan in 1976, 0.9 per cent subsequently revealed IlfV.'
Such low levels of infection may well have existed in other rural areas of the
equatorial region during the 197lls. They existed also in Kinshasa.
One of those testing positive at Yambuku had probably contracted lhc disease
in the capital during the early 1970s. Of 805 blood spccim..;ns taken from
pregnant women in Kinshasa in 1970. two later revealed HIV infection. So
did blood taken there in 1972 li:,om two of four patients with Kaposi's
s<Jrcmna2
The conversiun of this low-hovel infection into an expansive
probably took place in the urban envirumnent o!' Kinshasa during
The key may well have been the exceptional inftcrivity of the newly
which meant that if Llw virus entered a network nf sexual relationships in
which partners were exchanged rapidly and extensively. it could build up a
momentum of infection s11fficient to reach epidemic levels. That is
what happened in the UHiletl States. where HJV prevalence among homo-
sexnal men attending a sexually transmiltecl disease clinic in San Francisco
10
12 L:pidemic ill Westcm Equatorial :lfl'ica
rose between 1971\ am! 198'1 from l per cent to CS per cent.' it happened al hc~<iil of UNAIDS.' 'Meningitis was only mk manifc:-;iatiou of lhe disease,'
much the sarne period, although less explosively, among heterosexuah in the wru1e hb colleague Joseph McCormick:
East African cities of Bujumbura, Kigali, <md Nairobi, as al:,,, rural
south~weslcrn Uganda and in Abidjan in West Africa. The llrst occasion, how~ Some developed such cxquisHely son~ rrwuths and l<;llgues thdt they \Vere unable to
t'>vcr. wa~ in Kinshasa, INhere lllV first encountered rapid partner exchange in eat. Those 1-vhn conld nwnage a fo:~:-v bite:) of ~~)(Jd \Vere saddenb' strid\.en by LTL-unps
und disgorged a copious amouDI of diarrhea. T1wlr :)kin \A'ould break ont in massive.
urban sexual networks wider. although no! necessarily much more promis--
nwus, than lhose of the countryside. gL~nerahsed c.ruptll1ns. h1fect.cd fungating II1i:bSC.S vvould appear in::;ide and outside
The Hrst person to notice the change may well have beell Dr Kapila Bila, thdr buJies. \Vhen ihc infection didn'i cdnsisL of VU(.d._:luU'3 yeast cells las in
the Congolese physician heading the internal medicine department at Kin~ cryptococca1 nleningitis], there \Verc other parasites reaJy to cal the brain
shasa·s huge. 2.000-bed Mama Yerno Hospital. 'SometlJing dramatic happened alit'e. r·..Jone of the vklhns could ill auy 1:1lay \·vhat vvas happening to
in 19 7 5 ,' he recalled a decade later, referring especially to a doubling of cases I hem or why. c\.nd we? All we could do in horror, onr roles us physicians
reduced to scrupulous observers and accurale reL:urders uf Jocurnen.taliutL Our one
of Kaposi's sarcoma, a tumour !hat could take aggressive forms when the
immune system was damaged and hence often became a conspic:uons bope was thaL if we could und(Tstnnd the pC(:·U:0~,e~:; Vv'IC vverc observing. so1neone,
symptom of Aids. Other hospitals in the region observed this increase only in sontewhcre, ruight tlnd some solnUnn.10
the later 1970s and c<lrly 1980s, but Kspita Bila dated it at i\-lama Ycmo from Dh:guosing by :;ymptums, the teun.~ idcntiiied 30 .~\ids cases in Kim:hasa's
1975 and claimed lha! records revealed c<Jses at that time. The 20 men and 18 women. Of thesco. were l\otn Kinshasa itself. bul
records also conlirmed Congolc:;e doctors' recollections thut in the mid 19 70s others came from all parts of the country, indicating how far the virus had
they had first noticed numerous cases of 1b e severe wasting and diarrhoea that spread. On 3 November the team presented its tlnrlil:gs at a medit:al meeting
became the most common symptoms of Aids in Aldcan patients4 In the laic at Mama Yemo, warning !hat the disease appe<H<",ci to be sexually transmitted,
19 70s doctors across the river in Brazzaville observed similar cases. Physicians und fatal. 'If there a rnisfonut1e SJii\:.adiug terror in Kinshasa in
in Kinshasa initially attrilmtcd these symptoms to mbcrcu!osis, which spread the last few days, it is assuredly AIDS,' a locd1 wrote live days lc;ler. ·11.
epidemically in the region during the 1970s and 1980s, perhaps in synergy is ,;pnken of in the most v<;ried ways _ . ill l11e itt t!w rnurkcl, in bars, in
wiih HIV. By 1985, une~thinl of lnlx:rculosis patients in Kin.shasa's itospltab families ... Never in my memory as a jounwlb! l seen such concentration
also had IIIV.' l\ more distinctive indicator of Kinshasa's emerging HIV on a subject as disagreeable as strongly fc<1red .. , 1 H was hi:, last such
epidemic was cryptococcal meningitis, an agonising and commonly fatal comment, for President Mobutu's increasingly ul!popular and insecure govern~
infeciion of the brain. Hitherto generally confined to children, it spread in a ment banued the subject for the next four years. Fc>r the l(;ur million Kinois,'
distinctively urban form lo adults with damaged immune systems and became a {(Jreign journalist wrote in 1986, 'the disease, i<lck of dny olliclal int"onna~
increasingly common at Mama Yemo h-om the late 1970s.6 !iu:~, still has no name. Signs, therefore, suspicious. often infantile beliefs_ Aids
When blood taken in 1980-l from antenatal clinic attenders in Kinshasa all the same.' 12
was later tested, it showed that HfV prevalence among them had grown Heaciions abroad to evidence lhat the disease WdS widespread in a hetero~
during the 1970s from 0.2 per cent to 3 per cent7 The world's first HIV sexual pnpulatic,n vc;ere equally hostile. !\mcrkan medical journub rejected
epidemic among a heterosexual popnlation had begun before !he existence of l'iot's report and it took over a year tu convince the American government.
the virus was even suspected. That, more' than anything dse, was Africa Jn the meanlime the \1\'urld Health Orgauisutinn cauti,msly endorsed the
was to suffer so terribly during the following decades. Yet now discovery by French scientists that Aids was caused by a retrovirus.
came quickly. fn June l 981 American doctors published the flrst account of 1\·kCormick persunded the Centers for Disease Control in Atlanta to fund a
an epidemic of pnewnocystis carinii pneumonia among ;\mcrican homosexuals. research project in Kinshasa.n
On reading it, physicians in Brussels and Paris realised that they had treated Projet Sida, as it became known, began work in ]nne 19rH and defined tile
similar conditions since the mid l97Cls, chiefly in Africans li·mn the equatorial of tl:e urban disease in a form that still domin<Jied medical
region or Europeans who had visited iL Of the first 96 recorded Aids patients thought two decades later. A collaboration between American, Congolese, and
seen in Europe, 54 were Africans, 40 of them from the DR Congo-" In contrast Belgian specialists, initially led by an [,Jealistic public health expert named
to in!Ccted Americans, however, they 1vere heterosexuals in roughly equ<~l jonathan Mann, tbe Project bad nearly 300 staff at its peak and the
numbers of men and women, they did not take drugs, and they had no advantage of newly dccvised equipment to lcsl blood lix fliV. Its mosl
obvious risk factor in common except their geographical origin. In October important l1nding was that between 6 and 7 per cent of pr0gnant women at
1983 joint American and Belgian teams left li1r Kinshasa and KigalL Kinshasa's antenatal clinics were already infected with lllV, whereas earlier
At Mama Yemo, Kapita llila showed the visitors the palien!s he eslimatcs o[ lhc epidemic bad observed only the muc:h smaller numbers with
to be su!Iering from Aids. 'The moment [walked into the hospital in advanced Aids., Mann warned in 1986 that 'one to sever<~! milliun Africans
T realised something terrible was happening.' recalled Peter Piut, later may be infected'. He reckoned the annual incidence of new infections