Unresolved questions about HIV origins and emergence The discovery of the main HIV/SIV phylogenetic relationships permits explaining broad HIV
biogeography: the early centres of the
HIV-1 groups were in Central Africa, where the primate reservoirs of the related SIVcpz and SIVgor viruses (
chimpanzees and
gorillas) exist; similarly, the
HIV-2 groups had their centres in West Africa, where
sooty mangabeys, which harbour the related SIVsmm virus, exist. However, these relationships do not explain more detailed patterns of biogeography, such as why epidemic HIV-2 groups (A and B) only evolved in the
Ivory Coast, which is one of only six countries harbouring the sooty mangabey. It is also unclear why the SIVcpz endemic in the
chimpanzee subspecies
Pan troglodytes schweinfurthii (inhabiting the
Democratic Republic of Congo, Central African Republic,
Rwanda, Burundi,
Uganda, and
Tanzania) did not spawn an epidemic HIV-1 strain to humans, while the Democratic Republic of Congo was the main centre of HIV-1 group M, a virus descended from SIVcpz strains of a subspecies (
Pan troglodytes troglodytes) that does not exist in this country. It is clear that the several HIV-1 and HIV-2 strains descend from SIVcpz, SIVgor, and SIVsmm viruses,
Origin and epidemic emergence Several of the theories of HIV origin accept the established knowledge of the HIV/SIV phylogenetic relationships, and also accept that
bushmeat practice was the most likely cause of the initial transfer to humans. All of them propose that the simultaneous epidemic emergences of four HIV groups in the late 19th-early 20th century, and the lack of previous known emergences, are explained by new factor(s) that appeared in the relevant African regions in that timeframe. These new factor(s) would have acted either to increase human exposures to SIV, to help it to adapt to the human organism by
mutation (thus enhancing its between-humans transmissibility), or to cause an initial burst of transmissions crossing an
epidemiological threshold, and therefore increasing the probability of continued spread. Genetic studies of the virus suggested in 2008 that the most recent common ancestor of the HIV-1 M group dates back to the
Belgian Congo city of
Léopoldville (modern
Kinshasa), circa 1910. It is also believed that passengers riding on the region's Belgian railway trains were able to spread the virus to larger areas, combining with the active sex trade, rapid population growth and unsterilized needles used in health clinics to create what became the
African AIDS crisis. and many remained unmarried, This was accompanied by unprecedented increase in people's movements.
Michael Worobey and colleagues observed that the growth of cities probably played a role in the epidemic emergence of HIV, since the phylogenetic dating of the two older strains of
HIV-1 (groups M and O), suggest that these viruses started to spread soon after the main Central African colonial cities were founded. The workers in plantations, construction projects, and other colonial enterprises were supplied with
bushmeat, which would have contributed to an increase in hunting and, it follows, a higher incidence of human exposure to SIV. Several historical sources support the view that bushmeat hunting indeed increased, both because of the necessity to supply workers and because firearms became more widely available. The colonial authorities also gave many
vaccinations against
smallpox, and injections, of which many would be made without sterilising the equipment between uses. Chitnis
et al. proposed that both these
parenteral risks and the prostitution associated with forced labor camps could have caused serial transmission (or
serial passage) of SIV between humans (see discussion of this in the next section). The authors proposed that HIV-1 originated in the area of French Equatorial Africa in the early 20th century (when the colonial abuses and forced labor were at their peak). Later research established that these theories were mostly correct: HIV-1 groups M and O started to spread in humans in late 19th–early 20th century. alluding to
the book of the same title written by
Joseph Conrad, the main focus of which is colonial abuses in equatorial Africa.
Unsterile injections In several articles published since 2001, Preston Marx, Philip Alcabes, and
Ernest Drucker proposed that HIV emerged because of rapid serial human-to-human transmission of
SIV (after a
bushmeat hunter or handler became SIV-infected) through unsafe or unsterile injections. Although both Chitnis
et al. Unlike Marx
et al., The authors suggested that the very high prevalence of the
Hepatitis C virus in southern
Cameroon and forested areas of
French Equatorial Africa (around 40–50%) can be better explained by the unsterile injections used to treat
yaws, because this disease was much more prevalent than
syphilis,
trypanosomiasis, and
leprosy in these areas. They suggested that all these parenteral risks caused not only the massive spread of
Hepatitis C but also the spread of other
pathogens, and the emergence of
HIV-1: "the same procedures could have exponentially amplified HIV-1, from a single hunter/cook occupationally infected with SIVcpz to several thousand patients treated with arsenicals or other drugs, a threshold beyond which sexual transmission could prosper." the virus can be traced to a central African bush hunter in 1921, with colonial medical campaigns using improperly sterilized syringe and needles playing a key role in enabling a future epidemic. Pépin concludes that AIDS spread silently in Africa for decades, fueled by urbanization and prostitution since the initial cross-species infection. Pépin also claims that the virus was brought to the Americas by a Haitian teacher returning home from Zaire in the 1960s. Sex tourism and contaminated blood transfusion centers ultimately propelled AIDS to public consciousness in the 1980s and a worldwide pandemic.
Probable time interval of cross-species transfer Sousa
et al. use molecular dating techniques to estimate the time when each HIV group split from its closest
SIV lineage. Each HIV group necessarily crossed to humans between this time and the time when it started to spread (the time of the
MRCA), because after the MRCA certainly all lineages were already in humans, and before the split with the closest
simian strain, the lineage was in a simian. HIV-1 groups M and O split from their closest SIVs around 1931 and 1915, respectively. This information, together with the datations of the HIV groups' MRCAs, mean that all HIV groups likely crossed to humans in the early 20th century.
Male circumcision distribution and HIV origins Male
circumcision is not proven to reduce the probability of HIV acquisition by
men. Leaving aside
blood transfusions, the highest
HIV-1 transmissibility ever measured was from female prostitutes with 85% prevalence of HIV to uncircumcised men with GUD; 43% contracted HIV-1 after a single sexual exposure. There was no seroconversion in the absence of male GUD. Some
Bukusu communities in
Kenya have ceased circumcision because of a belief that the traditional form of the ritual can spread HIV.
Computer simulations of HIV emergence Sousa
et al. then built
computer simulations to test if an 'ill-adapted SIV' (meaning a
simian immunodeficiency virus already infecting a human but incapable of transmission beyond the short
acute infection period) could spread in colonial cities. The simulations used
parameters of sexual transmission obtained from the current HIV literature. They modelled people's 'sexual links', with different levels of sexual partner change among different categories of people (prostitutes, single women with several partners a year, married women, and men), according to data obtained from modern studies of sexual activity in African cities. The simulations let the parameters (city size, proportion of people married,
GUD frequency, male
circumcision frequency, and transmission parameters) vary, and explored several scenarios. Each scenario was run 1,000 times, to test the probability of SIV generating long chains of sexual transmission. The authors postulated that such long chains of sexual transmission were necessary for the SIV strain to adapt better to humans, becoming an HIV capable of further epidemic emergence. The main result was that
genital ulcer frequency was by far the most decisive factor. For the GUD levels prevailing in Léopoldville in the early 20th century, long chains of SIV transmission had a high probability. For the lower
GUD levels existing in the same city in the late 1950s (see above), they were much less likely. And without GUD (a situation typical of villages in forested equatorial Africa before
colonialism) SIV could not spread at all. City size was not an important factor. The authors propose that these findings explain the temporal patterns of HIV emergence: no HIV emerging in tens of thousands of years of human slaughtering of
apes and
monkeys, several HIV groups emerging in the nascent, GUD-riddled, colonial cities, and no epidemically successful HIV group emerging in mid-20th century, when GUD was more controlled, and cities were much bigger. Male
circumcision had little to moderate effect in their simulations, but, given the geographical
correlation found, the authors propose that it could have had an indirect role, either by increasing
genital ulcer disease itself (it is known that
syphilis,
chancroid, and several other GUDs have higher incidences in uncircumcised men), or by permitting further spread of the HIV strain, after the first chains of sexual transmission permitted
adaptation to the human organism. One of the main advantages of this theory is stressed by the authors: "It [the theory] also offers a conceptual simplicity because it proposes as causal factors for SIV adaptation to humans and initial spread the very same factors that most promote the continued spread of HIV nowadays: promiscuous [sic] sex, particularly involving sex workers, GUD, and possibly lack of circumcision." == Pathogenicity of SIV in non-human primates ==