Conceived and designed the experiments: JDdS VM PL AMV. Performed the experiments: VM PL. Analyzed the data: JDdS VM PL AMV. Wrote the paper: JDdS VM PL AMV.
The authors have declared that no competing interests exist.
The processes that permitted a few SIV strains to emerge epidemically as HIV groups remain elusive. Paradigmatic theories propose factors that may have facilitated adaptation to the human host (e.g., unsafe injections), none of which provide a coherent explanation for the timing, geographical origin, and scarcity of epidemic HIV strains. Our updated molecular clock analyses established relatively narrow time intervals (roughly 1880–1940) for major SIV transfers to humans. Factors that could favor HIV emergence in this time frame may have been genital ulcer disease (GUD), resulting in high HIV-1 transmissibility (4–43%), largely exceeding parenteral transmissibility; lack of male circumcision increasing male HIV infection risk; and gender-skewed city growth increasing sexual promiscuity. We surveyed colonial medical literature reporting incidences of GUD for the relevant regions, concentrating on cities, suffering less reporting biases than rural areas. Coinciding in time with the origin of the major HIV groups, colonial cities showed intense GUD outbreaks with incidences 1.5–2.5 orders of magnitude higher than in mid 20th century. We surveyed ethnographic literature, and concluded that male circumcision frequencies were lower in early 20th century than nowadays, with low rates correlating spatially with the emergence of HIV groups. We developed computer simulations to model the early spread of HIV-1 group M in Kinshasa before, during and after the estimated origin of the virus, using parameters derived from the colonial literature. These confirmed that the early 20th century was particularly permissive for the emergence of HIV by heterosexual transmission. The strongest potential facilitating factor was high GUD levels. Remarkably, the direct effects of city population size and circumcision frequency seemed relatively small. Our results suggest that intense GUD in promiscuous urban communities was the main factor driving HIV emergence. Low circumcision rates may have played a role, probably by their indirect effects on GUD.
Independent simian immunodeficiency virus (SIV) transfers to humans have established twelve different known human immunodeficiency virus (HIV) groups
Only four of these twelve strains generated successful epidemics in humans: HIV-1 groups M and O, and HIV-2 groups A and B. The pandemic group M strain clusters most closely with SIVcpz endemic in wild chimpanzees from the southeast corner of Cameroon
Transmission of simian retroviruses to humans is not exceptional. Simian foamy viruses (SFV) have frequently been transmitted to humans exposed to bushmeat, apparently without further spread
The estimated times of cross-species transmission to humans of the different HTLV-1 subtypes span between less than 3,000 and up to about 50,000 years ago
It is conceivable that host or circumstantial factors currently increasing the transmissibility of HIV were also involved in its origin and initial spread. This notion is implicit in the theories that proposed unsterile injections as the driving factor
Here, we aimed to identify which factors could have favored SIV adaptation to humans and facilitated its emergence and spread as HIV. First, we investigated the timing of the splits between HIV-1 groups M and O, and HIV-2 groups A and B and their respective closest SIV lineage, either by reviewing the literature or by using phylogenetic methods to narrow down the missing links. Having established a likely time interval of cross species transmission, we then reviewed colonial medical, and demographic literature, including original archival sources, to investigate how the proposed risk factors, including GUD incidence, city growth, health systems, gender distribution, and commercial sex work (CSW), varied in time and space, across the relevant African regions. Additionally we reviewed ethnographic literature on male circumcision per ethnic group, and assessed whether its geographical distribution, in early 20th century, overlapped with the putative epicenters for the HIV groups. Finally, we developed computer simulations based on detailed population, sociological and medical data found in our literature and archival searches to identify the key factors that might have facilitated the emergence of HIV-1 group M. Since spatial and temporal coincidence have previously been considered as evidence for factors involved in the emergence of a pathogen
We obtained divergence dates between epidemic HIVs and their closest simian relatives including recently discovered simian strains
The combined results are listed in
Calculation | Dating estimates | References |
Group TMRCA | 1920 (1902–39) |
Salemi et al. (2000) |
Group TMRCA | 1931 (1915–41) | Korber et al. (2000) |
Group TMRCA | 1921 (1908–33) |
Worobey et al. (2008) |
Split from closest SIV | 1853 (1799–1904) | Wertheim & Worobey (2009) |
Split from closest SIV | 1876 (1847–1907) | This study |
Group TMRCA | 1920 (1890–1940) | Lemey et al. (2004) |
Group TMRCA | 1905 (1866–1938) | Wertheim & Worobey (2009) |
Split from closest SIV | 1741 (1606–1870) | This study |
Group TMRCA | 1963 (1948–77) | Wertheim & Worobey (2009) |
Group TMRCA | 1940 (1924–56) | Lemey et al. (2003) |
Group TMRCA | 1932 (1906–55) | Wertheim & Worobey (2009) |
Split from closest SIV | 1889 (1856–1922) | Lemey et al. (2003) |
Group TMRCA | 1945 (1931–59) | Lemey et al. (2003) |
Group TMRCA | 1935 (1907–61) | Wertheim & Worobey (2009) |
Split from closest SIV | 1889 (1856–1922) | Lemey et al. (2003) |
Mean estimates and 95% credible/confidence intervals for group TMRCAs were obtained from previous studies, whereas divergence times from the closest SIVs were estimated in this study, and taken from
The five HIV groups represented in
The narrow time interval in which the four major HIV groups emerged, contrasting with the origins of HTLVs
To understand why only the early 20th century generated all epidemic HIVs, we aimed to reveal the full spectrum of factors that might have had the potential to increase SIV/HIV transmissibility and adaptation in the established critical time interval. In order to be consistent with a causal relationship, the factor or factors responsible should coincide both spatially and temporally with the origin of the epidemic
We reviewed colonial medicine articles, reports, and reviews, for the countries of chimpanzee and sooty mangabey ranges, searching for information about sexually transmitted diseases (STDs), GUDs, and diseases requiring intensive injection treatments (see
Primary and secondary syphilis (PSS) last a total of about five months, with exudative genital ulcers being present 30% of the time in either stage. This is followed by latent and tertiary stages, with no genital ulceration, and no infectiousness
In the relevant regions, the early 20th century witnessed very high GUD incidences especially in fast growing cities and socially changed semi-rural areas. This trend started around 1885, when European powers decidedly rushed to control the interior. Many sources explicitly state that syphilis was absent from nearly all forested areas where chimpanzees, gorillas, and sooty mangabeys live, up to 1885
In the period 1890–1920, colonization produced generalized social disruption, sex work flourished, and syphilis (and to a lesser extent chancroid and LGV) invaded all these areas
A common ironical pun was “
In Kinshasa (then Leopoldville), capital of the DRC (then Belgian Congo), GUD was much more intense in its early growth period, and then declined steadily after the mid 1930s (
Declines of 1.5–2.5 orders of magnitude happened between the 1920s and the 1950s. (Data compilation in
Starting to grow fast in 1919, the Kinshasa population tripled to about 47,000 by 1929
By 1928, there was a decided colonial response to these medical conditions. Mass surveys, movement restrictions, monitoring of sex workers and treatment of venereal diseases were initiated and were broadened further in scope and technically improved after 1932
Similar trends were observed in other African cities
Although we cannot exclude reporting biases concerning GUDs (or any other diseases) in colonial reports, these biases are likely to be less of an issue for cases detected in the major cities from the 1920s onwards, when health systems became better established. For this reason, we attempt to quantify GUD incidences only for cities, and from 1919 onward, despite having reviewed many other reports beyond these bounds.
Genital herpes (caused by the herpes simplex viruses (HSV), most often by HSV-2) plays a major role in HIV transmission nowadays, but its slow monotonic spread made it to be an important cause of genital ulcers in Africa only after the mid eighties
In summary, the period 1945–80 is characterized by a low intensity of the four main GUDs in major cities: PSS, chancroid, and LGV became rarer due to the better health systems, and penicillin use; PSS became a small fraction of treated syphilis cases; and genital herpes prevalence was still low. The incidences of the three former GUDs in cities showed peaks up to the mid thirties, when the cities were still small (10,000–50,000 inhabitants), sex ratios were very male-biased, and health systems were incipient.
City growth is a factor to be considered when investigating the emergence of epidemic HIV because a fast growing city potentially receives more SIV-infected migrants per unit time, and can spread the virus among more inhabitants. We examined the curves of population growth of the major Central and West African cities that lie within or near the chimpanzee, gorilla, or sooty mangabey ranges, and that received immigrants from within these ranges (
Plotted the evolution of the population of the most relevant cities at or near: (A) chimpanzee and gorilla ranges in Central Africa; (B) sooty mangabey range in West Africa. The supporting references are listed in
As
Both HIV-2 groups A and B originated most likely in Côte d'Ivoire
City growth is not restricted in time with the emergence of HIV groups. Cities continued to grow, well after the origin of the epidemic HIVs. While there is some spatial coincidence in Central Africa between city size and origin of HIV-1 groups, this is not the case for West Africa and the origin of the HIV-2 groups.
Male circumcision reduces the risk of HIV acquisition in men
We studied the geographical distribution of circumcision patterns in Central and West Africa both today and at the time of the HIV groups' TMRCAs, to evaluate if it correlated spatially and in time with HIV emergence. We reviewed all the Demographic and Health Surveys (DHS)
This near universality contrasts with what can be inferred from Murdock's Ethnographic Atlas
We found that, in the early 20th century, circumcision patterns in Central and West Africa exhibited much stronger regional differences than nowadays. Peoples of the Adamawa-Ubangi linguistic cluster (occupying most CAR and northern DRC), and many Bantu peoples of the Orientale and Équateur provinces of DRC, adopted it in late 19th–early 20th century
For the main cities of the relevant areas, we collected demographic surveys at several points in time which discriminated the urban population by ethnic group. To each ethnic group present in a city, at a given time, we assigned a “circumcision class” (e.g., generalized at puberty, absent, etc), based on the information provided in ethnographic sources, and we calculated upper and lower estimates of frequency of circumcision in male adults (see
The charts show, for each city, and at the referred time, the proportional distribution of the male population by “circumcision classes” which are directly derived from the ethnographic literature and do not depend on additional assumptions. Each bar is based on either: i) a published census or survey partitioning by ethnicity; ii) assumption of the same ethnic distribution as in a neighboring time point for which there is a census or survey; iii) published numbers for some ethnic groups, and estimates for some relevant others. The proportions of red and orange in each bar indicate the proportions of the population belonging to groups which, respectively had not adopted circumcision by the time of the data point (red), or had adopted it, or started to generalize it from a situation in which it is described as far from general in the ethnographic literature, less than 15 years before the time of the data point (orange). So, higher proportions of red and orange (and, to a lesser extent, pink) mean lower circumcision frequencies. See supporting information in
The charts show, for each city, and at the referred time, the upper and lower estimates of male circumcision frequency. The cities and times of estimates are the same that appear in the bars of
Among the three Central African cities which were clearly outstanding in size before the 1930s (Kinshasa, Douala, and Brazzaville (
Among the four West African cities that clearly stood out in size before World War II (Abidjan, Freetown, Monrovia, and Conakry (
To further substantiate these observations, we gathered tables of surgical operations discriminating circumcisions to treat phimosis and paraphimosis in major cities
Country | City/division | Years | # of cases | Annual incid. | Refs. |
Belgian Congo | Kinshasa | 1907, 1910–12 | 74 | 0.685% | |
Belgian Congo | Kinshasa | 1926 | 46 | 0.357% | |
Belgian Congo | Kinshasa, Matadi, Boma |
1930–31 | 245 | 0.395% | |
French Congo | Brazzaville | 1930–34 | 89 | 0.265% | |
Cameroon | Douala/Wouri |
1932, 1935 | 313 | 0.635% | |
Mali | Bamako | 1937 | 4 | 0.045% | |
Senegal | Saint Louis | 1937 | 6 | 0.040% |
Presented the joint annual incidences of phimosis and paraphimosis in the males of several African cities, as reported in the medical references listed in the last column. Demographic data for each city is in
The low incidences of phimosis in Mali and Senegal are explained by the Islamic practice of circumcision in childhood. The phimosis data support the findings of our ethnographic study that circumcision was far from general in Central Africa in 1910–35, and of lower rates in Kinshasa and Douala than in Brazzaville (
In our ethnographic study, we seized the opportunity to survey not only patterns of male circumcision, but also patterns of primate hunting. We present the results of this survey in
In conclusion, male circumcision rates in Central and West Africa were generally lower, and showed more pronounced regional differences in early 20th century than nowadays. Low circumcision levels in cities also appear to match early HIV epicenters and this is more evident for HIV-2 in West Africa than for HIV-1 in Central Africa.
Finally, we used computer simulations to verify that the time window for the emergence of epidemic/pandemic HIV strains indeed offered uniquely favorable conditions for the heterosexual spread of the virus. Because the window of opportunity may have involved simultaneous changes in several factors (population size, sex ratio, sexual promiscuity, GUD and circumcision prevalence), we also wanted to evaluate the individual contribution of each factor to successful epidemic emergence.
We focused on the origin of HIV-1 group M in Kinshasa for which we were able to collect the most complete historical data. Our simulations were parameterized to follow the recorded population size and structure of Kinshasa at several relevant time points, partly based on the availability of detailed population and medical records (
Parameter | Pre-colonial village | Kinshasa 1919 | Kinshasa 1929 | Kinshasa 1958 |
Number of women | 500 | 3,265 | 10,081 | 69,159 |
Number of men | 500 | 8,798 | 31,817 | 93,064 |
Number of married couples | 450 | 947 | 2,923 | 48,411 |
% of women “ |
0 | 60 | 60 | 10 |
% of men circumcised | 0 | 70 | 80 | 95 |
Genital ulcer frequency (%) in: | ||||
Commercial sex workers (CSWs) | - | 15 | 10 | 5 |
0 | 7.5 | 5 |
0.5 | |
Other women | 0 | 3 | 2 | 0.3 |
Men | 0 | 1.5 | 1 | 0.3 |
The parameters are based on archival historical data and colonial medicine articles (
Our simulations followed the early spread of the epidemic from the first zoonotic SIV infection over a dynamic network of sexual contacts, which was parameterized according to recent surveys
Parameter (notation) | Default value/Formula [references] | Other values tested [references] |
Number of non-spousal partners per year |
||
Single women (NSW) | 1.5 |
|
Married women (NMW) | 0.2 (estimated from data in |
|
Single men (NSM) | 3 |
4.5 |
Duration of short links |
52 (in |
26 |
Number of sex acts per week |
||
Stable (spousal) link | 2 |
|
Short link | 0.24 (estimated from data in |
2 |
CSW visits per man per year |
2 |
0 |
Sex acts per CSW per year (SC) | 600 |
150 |
Probability of short link breakup per week (pb) | 1/D | |
Probability of short link formation | ||
Single women | NSW/(D+52) | |
Married women | NSM/(D+52) | |
Single men (pf,SM) | NSM/(D+52) | |
Married men |
pf,SM–pb | |
Number of CSW | (Number of men)*C/SC | |
Probability of CSW visit per man per week | C/52 | |
Duration of acute infection (weeks) | 12 |
|
Transmission multiplier for acute infection | 10 | 4, 26 (estimate for modern HIV-1 |
Maximum per-act transmission probability | 0.9 | 0.43 (equal to highest observed heterosexual rate |
Per-act transmission probabilities |
||
♂→♀ and ♀→♂(C) | 0.001 |
|
♀→♂(NC) | 0.0025 |
0.01 |
♂→♀(GU) | 0.07 |
|
♂(GU)→♀ and ♀(GU) →♂(C) | 0.04 |
|
♀ (GU) →♂(NC) | 0.43 |
|
♀ →♂(GU) | 0.023 | |
♂(GU)→♀(GU) and ♀(GU)→♂(GU) | 0.43 | |
Duration of GU episodes (weeks) | 10 |
We defined several markers to characterize the efficiency of epidemic spread in the simulations (
The graphs depict frequency distributions of the total number of infections per simulation (A), the duration of the epidemic (B) and the longest chain of transmission (C) from 1,000 simulations of Kinshasa in 1919 (red dots and bars), 1929 (blue dots and bars) and 1958 (green dots and bars), and a pre-colonial village (black dots and bars). The duration of an epidemic was defined as the time until the resolution of the last acute infection: its lower bound was defined by the length of acute infection in patient zero (12 weeks), its upper bound by the length of the simulations (52 weeks). The longest transmission chain was defined as the number of individuals in the longest chain of subsequent transmissions in each simulation. All frequencies (number of observations) are plotted on a log scale.
In all three quantifiers of epidemic emergence, the performance of the historical scenarios followed the same pattern: Kinshasa 1919> Kinshasa 1929≫ Kinshasa 1958≫ pre-colonial village (
While the resistance of the pre-colonial village to HIV emergence is not surprising, the dramatic decrease in permissiveness between 1929 and 1958, in spite of continued explosive population growth, demands further explanation. Furthermore, the 1919 scenario proved to be consistently more permissive than the 1929 scenario, in spite of considerable population growth over the decade. To identify the key factor(s) behind the observed differences, we explored systematically the effect of removing or reducing several factors that have been implicated in the emergence of HIV. Based on the most permissive 1919 scenario, we tested 10-fold reduced population size, balanced sex ratio (with 90% of the sexually active population in stable relationship), absence of GUD infections and universal circumcision. The removal of GUD infections proved to have by far the most dramatic effect (
The graphs depict frequency distributions of the total number of infections (A), the duration of the epidemic (B) and the longest chain of transmission (C) from 1,000 simulations of Kinshasa with default parameters (black dots and bars), 10-fold reduced population size (red dots and bars), balanced sex ratio (blue dots and bars), no GUD (green dots and bars) and universal circumcision (gray dots and bars). The duration of an epidemic was defined as the time until the resolution of the last acute infection: its lower bound was defined by the length of acute infection in patient zero (12 weeks), its upper bound by the length of the simulations (52 weeks). The longest transmission chain was defined as the number of individuals in the longest chain of subsequent transmissions in each simulation. All frequencies (number of observations) are plotted on a log scale.
We present multiple lines of evidence favorable to the hypothesis of rampant GUD epidemics having played a key role in the origin of the major HIV strains.
In agreement with earlier studies our molecular dating confirmed that all major epidemic HIV lineages were transmitted to our species in a narrow time frame. We dated the divergence of the HIV-1 groups M and O from their closest related SIVs using a different, but complementary approach compared to Wertheim and Worobey (2009)
Thus, we looked for factors to explain why emergence of HIV is temporally and spatially restricted to the era and areas observed. Our review of the co-factors of sexual transmission indicated GUD as paramount and lack of male circumcision of secondary importance. GUD provides a portal of entry and attracts cells carrying CCR5, the co-receptor most used by HIVs and SIVs upon sexual transmission. In addition, GUD and especially syphilis induces a potent inflammatory response, and tumor-necrosis-factor (TNF)-α production
Most theories for the origin of HIVs depend on a specific mechanism to facilitate the first few serial transmissions of the virus in humans, and largely limit the problem to initial adaptation
Our computer simulations of detailed historical scenarios for Kinshasa confirmed that the period around the origin of HIV-1 group M in the city was uniquely permissive for the emergence of an epidemic by heterosexual transmission. While exact probabilities of HIV emergence cannot be computed (e.g. we have no information on the initial infectivity of a novel zoonotic HIV), our semi-quantitative approach could robustly predict an increased relative probability associated with this time period. Furthermore, our simulations suggested that the peak in GUD prevalence was the most important contributor to chains of transmission of ill-adapted HIV. A related important result of the simulations is the inability of zoonotic HIV to generate epidemics in the pre-colonial village scenario (characterized by the absence of GUD and CSWs), which explains the long standing absence of HIV epidemics in the pre-colonial environments. According to these results, the window of high permissivity for epidemic HIV emergence was open by the spread of GUD infections due to the organized colonization of the relevant African areas, and probably closed by the aggressive treatment campaigns against GUDs from the mid thirties. Therefore, we predict that newly emerging HIV groups will have a less dramatic spread if GUD remains under control. Remarkably, the direct effect of population size and circumcision proved to be relatively small, although their effect is recognized and they may have acted indirectly.
In the simulations, the probabilities for sexual link formation and breakup were the same for all individuals of a class (e.g. single men, married women, etc). For the sake of simplicity, we did not implement a “small world network”
Simulation models have been used before to estimate the contribution of sexually transmitted infections/GUDs to the current heterosexual spread of HIV
We hypothesized that differences in male circumcision levels between cities may help to explain why HIV zoonotic strains emerged only in particular countries. Our extensive survey revealed circumcision patterns that were historically low in the putative centers of HIV emergence (Kinshasa, Douala, and Abidjan). Our simulations showed only a moderate direct effect of circumcision in the probability of generating long chains of transmission. However, lack of circumcision also favors GUD transmission
Independently of the regional differences encountered, our finding of a very widespread trend of adoptions of circumcision, in early 20th century, by ethnic groups previously not practicing it, and the resulting temporal increase of circumcision rates in most relevant countries, is a solid result. It explains, as far as we know for the first time, the discrepancy between modern levels of circumcision, as showed by the Demographic and Health Surveys (DHS)
Independent of whether lack of circumcision was important to HIV adaptation, its geographical distribution may have determined to a large extent, which secondary foci developed in the decades after early emergence. Our finding of a relatively low circumcision rate in Guinea-Bissau may reinvigorate the debate about why this country became an early important focus of HIV-2 group A. In this regard it is important to note that some of the earliest transnational jumps of pandemic HIV-1 happened to countries where circumcision is uncommon: Haiti
Our simulations suggest that city size
Third, while initial bursts of SIV spread, and resulting adaptation, might have happened in small settlements, further spread of the epidemic was probably centered on cities with large populations. Large cities were at the center of star-like traffic networks, connecting them to nearby settlements, and allowing for quick transfer of the virus from a local initial outbreak. Furthermore, outbreaks in small settlements might quickly become self-limiting by exhausting the supply of susceptible individuals, and sustained epidemics probably depended on the early transmission of the virus to a large center with fast replenishment of susceptible individuals to maintain the epidemic. Thus, major, well-connected centers, such as Kinshasa and Douala (which were better served by railway and fluvial connections, and had far more traffic than the other cities), may have acted as an “attractor” and a “hub” for HIV epidemics. Although these ideas were not explicitly modeled in this study, they may help to understand why exactly two HIV-1 strains evolved and spread considerably in Central Africa, and perhaps may give clues on the origin of the subtypes.
Our proposal that Kinshasa, Douala, and Abidjan constituted the initial hubs of the epidemic HIV groups can also explain the following historical facts: 1) the presence of already diversified HIV-1 group M in Kinshasa in 1959–60, as evidenced by two seropositive samples (a subtype B/D and a subtype A) in only a few hundred stored blood and tissue samples available for screening
Our hypothesis satisfies both temporal and spatial coincidence between the factors which we invoke and the emergence of a pathogen. Such coincidence has previously been considered evidence that the factors are causally implicated
In this study, we narrowed down the origin of the epidemic HIV clades (HIV-1 groups M and O, HIV-2 groups A and B) to the first half of the 20th century, using phylogenetic molecular clock calculations. Our colonial archival literature survey shows that GUD epidemics peaked in cities in their early phases of development, providing a better coincidence with this narrow time frame than the driving factors proposed by other theories. Ethnographic literature illustrates that circumcision frequencies were historically considerably lower, and spatially more variable, than they are currently; in particular for HIV-2, low circumcision prevalence in cities indeed showed a geographical match with emerging HIV epicenters. Through epidemiological modeling we could simulate that early ill-adapted HIV could generate long chains of transmission only during a period of high GUD intensity. The effects of circumcision and city size were more likely indirect, through their capacity to enhance GUD intensity and allowing the initial hub of infections to potentially reach a threshold, and to spawn secondary foci. We conclude that intense GUD in nascent cities was probably the main factor that permitted zoonotic SIV to emerge as epidemic HIV, possibly in association with low circumcision rates.
We hope our hypothesis will increase awareness of the dangers posed by GUD in promoting transfer of SIV, STLV, and possibly other sexually transmitted viruses, to our species. These observations recommend close monitoring and treatment of GUD in Africa, and raise concern over the currently high prevalence of HSV-2 associated genital ulcers. We also underscore the importance of male circumcision in the prevention of novel HIV strain emergence.
SIVcpz–HIV-1 group M and SIVgor–HIV-1 group O divergence dates were estimated using a Bayesian relaxed clock analysis implemented in BEAST
We compiled STD and GUD incidence data for all the countries at or near the ranges of chimpanzees and sooty mangabeys through a survey of the relevant literature, of the period 1890–1960, from the following sources:
1) Official colonial reports about health, or containing sections about health, and covering also demographic issues. A) For the Belgian Congo, collected in the Afrika Archief, Federale Overheidsdients–Buitenlandse Zaken, Buitenlandse Handel en Ontwikkelingssamenwerking (FO-BZBHO) (Ministry of Foreign Affairs), Brussels; B) For French Equatorial Africa (AEF), and French West Africa (AOF), collected in the Centre des Archives d'Outre-Mer (CAOM), Aix-en-Provence (France), and in the Institut de Médecine Tropicale du Service de Santé des Armées (IMTSSA), Marseille (France).
2) We complemented this information with articles in the main colonial and tropical medicine journals (Ann Méd Pharm Coloniales, Ann Hyg Méd Coloniales, Ann Soc Belge Méd Trop, Bull Soc Pathol Exotique, West African Med J, and others), and with books on the subject.
We did a complete survey of the GUD incidences in Kinshasa: supporting data and methods are described in
We obtained the relevant demographic data about the relevant cities from articles, books, and archival reports (references in
We obtained circumcision information on ethnic groups from the Revised Ethnographic Atlas (Gray (1999)
We developed a stochastic, individual-based simulation model to track the initial spread of HIV over a dynamic network of sexual contacts. The model distinguished married and single men and women, “
Simulations had a time step of one week. All runs were preceded by an initialization phase restricted to link formation and breakup until the sexual network settled to a steady state. The initial HIV infection was then introduced into a single male to reflect the most likely source of a bushmeat hunter, and the spread of the virus was followed for a year. At each time step, sexual contacts were generated randomly over stable and short links; CSW visits involved a single sexual contact. HIV transmission was restricted to acute infection; its probability per contact was modified by GUD and circumcision status. Transmission rates were scaled according to estimates on modern HIV (
The biogeography of epidemic HIV strains in Central Africa (A), and West Africa (B). The ranges of the primates that were the source of SIVs that gave rise to HIV strains are indicated (based on
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Modern levels of male circumcision in relevant countries of Central and West Africa.
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The coverage of male circumcision information attained by our ethnographic survey.
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Killing and consumption of apes/monkeys in Central and West Africa.
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Summary of the simulations outcomes for the four historical scenarios.
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Summary of simulation outcomes for combinatorial variants of the Kinshasa 1919 scenario.
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GUD incidences in Leopoldville/Kinshasa.
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Circumcision prevalences in Central and West Africa.
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Source code of the simulations.
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Circumcision classes and frequencies in Central and West African cities.
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We are grateful to Prof Emeritus Jozef Vandepitte (Katholieke Universiteit Leuven, Belgium), to Prof Emeritus Stefaan Pattyn, (Tropical Institute of Medicine, Antwerp, Belgium), to Father Honoré Vinck and Prof Motingea Mangulu (Aequatoria, Belgium, and Democratic Republic of Congo), and to Prof Tamara Giles-Vernick (Univ of Minnesotta), for enlightening discussions. We thank Prof Charles Becker (Centre National de Recherche Scientifique, France), for guidance over the use of French colonial archives, Prof Barry Hewlett (Univ of Vancouver, Canada) for having provided us his original ethnographic dataset. We thank Drs Pierre Dandoy and Rafael Storme (Afrika Archief, Federale Overheidsdients–Buitenlandse Zaken, Buitenlandse Handel en Ontwikkelingssamenwerking (FO-BZBHO), Brussels), Dr Evelyne Camara (Centre des Archives d'Outre-Mer (CAOM), Aix-en-Provence, France), and Dr Aline Pueyo (Institut de Médecine Tropicale du Service de Santé des Armées (IMTSSA), Marseille, France), for their attention and help to our research in their respective Archives.