The Origins of AIDS (29 page)

BOOK: The Origins of AIDS
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Such an initial phase of parenteral amplification was necessary for the emergence of
HIV-2 in West Africa, a virus whose sexual transmission is rather ineffective but which still managed to infect tens of thousands of individuals, as summarised in
Chapter 10
.
HIV-2 slowly faded away when the opportunities for its parenteral transmission decreased: the number of newly infected subjects ultimately became less than the number of long-infected individuals who died of AIDS or some other disease. This contrasts with
HIV-1 group M which, after benefiting from the parenteral amplification, also proved its superior ability to infect lymphocytes and other cells, a characteristic that would facilitate its sexual transmission. Part of the epidemiological success story of HIV-1 group M was thus probably biological and intrinsic to this virus. HIV-1 group N did not benefit from such parenteral amplification, because it crossed species in a more recent era when IV drugs had been replaced by oral meds for the treatment of many tropical diseases, with the result that it remained limited to a very small number of infected individuals.
While the initial phase of parenteral amplification of HIV-1 group M must have occurred in an area inhabited by
P.t. troglodytes
, the next phase of sexual dissemination followed migration and trading routes
. From a rural area, HIV-1 moved into the nascent cities of central Africa. On a purely geographic basis, the most likely candidates for such urban spread were Yaoundé, Douala, Libreville, Bangui, Brazzaville and Léopoldville.
However, given the very low HIV-1 prevalence measured in Cameroonian and Gabonese cities in the mid-1980s, among the general adult population but also sex workers (
Chapter 13
), the early sexual propagation probably did not occur there. The clear preponderance in Cameroon and Gabon of CRF02A_G
, a recombinant which could not have emerged in the early years of the epidemic, further rules
out these locations as the site of the initial spread.
We cannot rule out Bangui, where prevalence was already a significant 4.4% in 1986. It is unfortunate that no archival serum samples from Bangui or southern
Central African Republic were ever found in the local Institut
Pasteur or that if such work was done it was not published.
The lower genetic diversity of HIV-1 subtypes in Bangui compared to Kinshasa and Brazzaville (
Chapter 1
) suggests that the virus has been circulating in the latter area for a longer period of time than on the banks of the
Oubangui. Furthermore, only a small part of the Central African Republic is inhabited by
P.t.
troglodytes
and the genetic diversity of HIV-1 is similar to that in
Chad, a country without any
P.t. troglodytes
. These two countries’ intermediate genetic diversity of HIV-1 isolates probably represents an ancient import of subtypes which had already been differentiating somewhere else
.
5

6
Several arguments suggest that the Léopoldville/Brazzaville urban area was central in the dissemination of HIV-1 (
Chapters 1
and
13
). First, the extraordinary diversity of HIV-1 in samples obtained from Kinshasa and Brazzaville, where all known subtypes and many recombinants are present. Second, the two oldest samples containing HIV-1 obtained in 1959–60 both came from Léopoldville. Third, the retrospective description of five clear-cut cases of AIDS that corresponded to infections probably acquired in the DRC in the late 1960s or early 1970s. Fourth, the presence of HIV-1 antibodies in samples obtained in 1970 from women representing the general adult population of Kinshasa (mothers bringing their children to an under-five clinic), even if at a low prevalence of 0.25%. Fifth is the finding that in 1980, among a similar sample of women, prevalence was already at 3.0%. Sixth, the surveys conducted in representative samples of the adult population of various central African cities in the mid-1980s showed low prevalences in
Gabon and Cameroon but rather high prevalences (4–8%) in Kinshasa and Brazzaville
. Finally, the status of the Léopoldville/Brazzaville conurbation, for a long time the commercial and administrative heart of central Africa attracting thousands of
migrants each year into an ever larger melting pot of all ethnic groups
.
7

15
What was the geographical origin of the first cases of HIV-1 imported into Léopoldville/Brazzaville? There is a remote possibility that the source was from within the Belgian Congo. The part of the
Bas-Congo region north of the river was inhabited by
P.t. troglodytes
, and there were
excellent road and rail communications between Boma, Matadi and Léopoldville. However, this area is small, with limited
P.t.
troglodytes
populations, and we do not know whether local communities of chimps are infected with SIV
cpz
. Far more likely, the virus managed to reach Brazzaville first, with its subsequent implantation in Léopoldville just across the river. As reviewed in
Chapter 5
, Brazzaville became the administrative centre of the
AEF
federation, the terminus for navigation on the Congo and the departure point of the train to
Pointe-Noire and the Atlantic coast. These factors implied constant movements of Africans and Europeans between the capital city and the territories of
Oubangui-Chari,
Moyen-Congo and
Gabon. Initially concentrated within Moyen-Congo, these population movements reached further inland and on a massive scale when forced labour was brought in for the construction of the
Congo–Océan railway in the 1920s.
Furthermore, the part of south-east Cameroun with the highest prevalence of SIV
cpz
among its chimps, and whose strains of SIV
cpz
are closest to
HIV-1 group M, has rivers, the
Dja and the
Ngoko, that drain into the Congo system through the
Sangha
, which also drains part of southern Oubangui-Chari inhabited by
P.t.
troglodytes
.
For these populations, trading was easier towards the Congo than to
Yaoundé and Douala, and ever since the German colonisation, steamboats would regularly make the journey between south-east
Cameroon and Brazzaville/Léopoldville
.
Once HIV-1 reached Brazzaville, it would not take long for it to move into Léopoldville. Some traders from the AEF hinterland visited both cities on the same or successive journeys, depending on where they thought they could fetch the highest prices for their goods. Alternatively, there might have been a little local transmission within Brazzaville before the virus was introduced into Léopoldville. There was a ferry as well as smaller boats departing every half hour for the twenty-minute journey. Before independence, commerce was brisk between the two cities, as traders, many of them women, managed to find a price differential for some goods that would make the short trip profitable. And after independence in 1960, when the economic situation deteriorated in the DRC, trading if anything increased as agricultural products from the
Bas-Congo could be sold at higher prices in Brazzaville, where smart traders could then use their CFA francs to buy goods that Léopoldville was short of, guaranteeing a hefty profit.
Free women also moved back and forth between the two capitals while other
migrants settled on the other side of the river for longer periods in search of a better life (
Chapters 5
and
6
)
.
16
Once HIV-1 was present in both cities, the conditions in Léopoldville were more favourable to its successful sexual propagation than in Brazzaville. Early in colonial history, a gross gender imbalance was created in Léopoldville by the Belgian colonists, on a scale far worse than across the river, as we have examined in
Chapter 5
. For a few decades, Léopoldville was an urban work camp where women and children were unwelcome. This was fertile ground for prostitution to develop on a large scale, and develop it did.
Even when colonial policies were softened after WWII, Léopoldville was such a booming town that it constantly attracted a flux of migrants from the adjacent rural areas and young men would come first, perpetuating the imbalance
. On both sides of the trade, prostitution involved mainly the unmarried and within this subgroup as late as the 1950s there were more than five men for each woman in Léopoldville.
For the first few decades of its presence in Léopoldville, the dissemination of HIV-1 was slow and limited. According to mathematical models, for a long time there was something like 100 infected individuals in the city (
Chapter 3
). The type of sex trade that existed during the colonial era corresponded to what is currently referred to as concomitant partnerships or semi-prostitution rather than hard-core prostitution (
Chapter 6
). A free woman would have a few regular clients, perhaps three on average, to whom she provided a variety of services, not just sex. If that woman got infected with HIV-1, she could only transmit the virus to one of her other steady clients, who might eventually infect another free woman. This setting was good enough for the persistence of the infection, possibly a very slow growth of the infected population up to a few hundred, but nothing like the exponential transmission of HIV-1 that was to be documented in Kenya in the early 1980s.
It is likely that some of the initial transmission of HIV-1 to free women in Léopoldville occurred iatrogenically and not just sexually. For a long time, starting in the early 1930s, free women were forced to attend the
Dispensaire Antivénérien in Léo-Est for regular STD screening (
Chapter 9
).
Those with a positive syphilis serology (many of whom carried such antibodies not because of syphilis but because they had had yaws in their childhood) were treated with injectable drugs, most often administered IV. In 1953, more than 150,000 injections were administered just in this one institution, which treated up to 1,000 patients each
day
. Documentary evidence reveals that syringes and needles were not sterilised but only rinsed between patients, with the result that many cases of iatrogenic hepatitis
B acquired in this STD clinic were recognised by a clinician at the main hospital of Léopoldville, even in a setting where only a small minority of adults was susceptible to infection with HBV. This situation created an extraordinary opportunity for the spread of HIV-1: the women infected iatrogenically were semi-prostitutes, who could in turn transmit the infection, now sexually, to some of their regular clients. And thus a perfect storm developed.
17
More widespread sexual transmission became possible when the face of prostitution in Léopoldville was dramatically altered around 1960–1. The political chaos and civil war in parts of the Congo brought hundreds of thousands of internal refugees into the capital, resulting in massive unemployment and poverty (
Chapter 11
). As documented by several observers, high-risk prostitution appeared, with sex workers providing sexual services to a few men every day, potentially more than 1,000 per year, in downmarket brothels which were little more than glorified shacks. For a number of years, it remained a concentrated epidemic, with a higher prevalence among prostitutes than among their clients. As long as the gender imbalance persisted, that is until the early 1970s, there were relatively few opportunities for dissemination outside this initial core group, because for many men it was not easy to find a female partner to marry or with whom they could at least sustain a romantic relationship
.
The transition from a concentrated to a generalised epidemic occurred between 1970 and 1980, a period during which HIV prevalence among mothers at a well-baby clinic in Kinshasa increased from 0.25 to 3.0%. If these prevalences were representative of the whole adult population of Kinshasa, the number of HIV-1-infected individuals in the city rose from about 1,400 in 1970 to some 36,000 ten years later. That is why in the mid- to late 1970s physicians at the Mama Yemo and at the university hospitals started seeing cases of what would be later recognised retrospectively as AIDS
.
13
,
14
,
18

21
Once the number of HIV-infected persons in Léopoldville expanded, it was unavoidable that it would spread outside the capital, which was the political and economic centre of a large country with endless movement of traders, bureaucrats and all kinds of economic migrants between the various regions of the Belgian Congo, the DRC and later Zaire. HIV-1 eventually reached
Kigali,
Rwanda, where it found extremely favourable conditions for its sexual transmission in this
small city with a gross surplus of uncircumcised men and a thriving sex industry (
Chapter 13
). A similar process, albeit with a different founder strain, happened in
Bujumbura,
Burundi. In other countries of central Africa, HIV-1 arrived at the same time or even earlier, but as conditions were less propitious its spread was slower. From central Africa, HIV then progressively moved into other regions of the continent. Southern Africa was infected by the extension of subtype C infection from the
Katanga province of the DRC to
Zambia, and then further south to
Zimbabwe,
Malawi and eventually
South Africa. East Africa was infected via
Kisangani while West Africa was infected by the extension of the
CRF02A_G recombinant northwards along the coast, from
Gabon and
Cameroon to
Nigeria,
Ivory Coast and so on.

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