Where did HIV come from?

An infection that began in animals

Human immunodeficiency virus is a zoonosis – an infection that originated in animals and passed into human hosts.

Human immunodeficiency virus is closely related to the simian immunodeficiency virus (SIV) found in chimpanzees in central Africa. This virus is called SIVcpz to distinguish it from forms of SIV less closely related to HIV, found in other primates. (Sharp) SIVcpz causes an AIDS-like illness in chimpanzees. (Keele)

SIVcpz is found in wild chimpanzees of two species (Pan troglodytes troglodytes and P. troglodytes schweinfurthii) in southern Cameroon and north-eastern Gabon, as well as in small groups in western Tanzania and the eastern Democratic Republic of the Congo (DRC). Another form, SIVsmm, is found in sooty mangabey monkeys and is closely related to HIV-2.  

SIV probably entered the human population as a result of hunting and butchering chimpanzees. It is plausible that transmission could have occurred through a hunter being wounded and blood from a chimpanzee entering his bloodstream. Chimpanzees avoid humans wherever possible, so it is likely that SIVcpz crossed into humans as a result of human encroachment into forest areas. European colonisation of equatorial Africa in the late 19th century led to the exploitation of previously untouched rainforests for the farming of rubber and other commodities.

There are two major types of the human immunodeficiency virus: HIV-1 and HIV-2. The most widespread type is HIV-1, which can be further divided into four groups. Each group is thought to represent one virus transfer from a primate to a human and all viruses in the group are descended from that transfer:

• Group M is the predominant form and accounts for almost all HIV-1 infections that have occurred.
• Group N has been found in a small number of people in Cameroon.
• Group O has been found in small numbers of people in Cameroon, Gabon and Congo.
• Group P has been found in a Cameroonian woman in France. It is closely related to SIVgor, a form of SIV found in gorillas in a small area of southwestern Cameroon. (D’arc)

HIV-2

HIV-2 is similar to HIV-1 but causes severe immune deficiency less often. (Campbell-Yesufu)

HIV-2 originated in sooty mangabey monkeys in west Africa. It is descended from SIVsmm, a form of SIV that is similar to SIVcpz. Using the same techniques as for HIV-1, researchers estimate that the two major groups of HIV-2 entered the human population around 1940. (Wertheim) At least eight separate groups of HIV-2 have been identified, suggesting that numerous transfers have taken place.

Less easily transmitted during sexual intercourse, HIV-2 infection seems to have spread in west Africa mainly through the use of non-sterile needles and syringes to administer injectable treatments for sleeping sickness and tuberculosis. (Pépin, pp 247-50)

Where did HIV-1 start?

The most significant transfer, of the ancestor of HIV-1 Group M, may have occurred in south-east Cameroon. Episodes of SIVcpz transfer from chimpanzees to humans were likely to have been rare events, due to the low probability of transmission from chimpanzee blood to the human bloodstream. Chimpanzee hunting was rare before the arrival of firearms in the region in the early 20th century. One study has suggested that chimpanzee hunting intensified during the First World War when a Franco-Belgian occupying force seized southern Cameroon from the German occupiers. (Pépin, p 300)

Several scenarios have been proposed for the subsequent dissemination of the HIV-1 Group M ancestor from south-east Cameroon. Re-use of glass syringes used to treat sleeping sickness is one way in which the virus could have passed to others in Cameroon. HIV-1 Group M might then have been carried by a traveller on the Sangha river, which connects the region to Leopoldville (now Kinshasa). Another possible route is through the evacuation of the Franco-Belgian occupying force from south-east Cameroon to Leopoldville, the capital of Belgian Congo (now DRC), and Brazzaville, the capital of French Congo (now Congo). (Pépin, pp 296-302)

A study of HIV evolution, based on the earliest known sample of HIV dating from 1959, has estimated that HIV introduction and the divergence of HIV group M into various sub-types occurred during the 1940s or 1950s. (Zhu)

Subsequent studies of samples of HIV group M collected in Leopoldville in 1959 and 1960 confirm that the virus had already evolved into subtypes by this time. (Worobey) By looking at an intact sequence of HIV from a lymph node tissue sample stored in 1959 and knowing the rate at which HIV mutates each year, scientists have estimated that HIV group M is descended from SIVcpz that entered humans between 1890 and 1920. (Faria)

However, all estimates of the crossover date depend on the accuracy of the ‘molecular clock’ method used to calculate a crossover date. This method assumes that HIV mutates at a constant rate. Some scientists have criticised its use because it excludes the effects of the recombination of viruses – the swapping of genetic material between viruses – on the evolution of HIV’s genetic code. However, a recent study which allowed for this effect concluded that HIV-1 group M entered humans in the 1920s. (Olabode)

What caused HIV to spread?

If HIV-1 Group M reached the human population by the 1920s, why did it take so long to spread more widely? Isolated cases suggestive of AIDS before 1981 have been identified in Europe and North America with the aid of retrospective analysis of stored samples, but it has been difficult to detect cases in central Africa before the 1980s. The first probable cases of AIDS were documented in Zaire (now DRC) and Rwanda in 1977. (Vandepitte; Rogan) Also, no HIV has been found in tissue samples stored before 1959 in central Africa.

Looking at HIV diversity in the earliest samples, one study has estimated that fewer than a hundred people were living with HIV before the mid-1950s. (Worobey) Several factors seem to have created an environment in which HIV could spread more easily from the 1950s onwards in Leopoldville (now Kinshasa), the capital of Belgian Congo:

• More frequent use of injections in medical treatment. Injectable arsenic-based treatments were used to treat syphilis. A clinic used by the city’s sex workers gave up to 300 injections a day during the 1950s, many of them with reused unsterilised needles and syringes. Cases of hepatitis after injectable treatments were documented at this clinic in 1953, suggesting HIV could have been transmitted in the same way. (Pépin, pp 223-30)
• The pattern of sex work changed in the city. The civil unrest, population growth and unemployment that followed independence in 1960 led to a refugee crisis in the city. Sex work became more common among women in the city and their client numbers increased. (Pépin, pp 148-52)  
• Changes in the virus. The virus which reached the city is more transmissible than HIV-1 groups N, O or P. Also, experiments in humanised mice have shown that SIVcpz is less likely to kill CD4 cells than HIV-1 group M, suggesting that HIV-1 may have mutated after entering humans to become more harmful. (Yuan) Greater transmission and passage through human hosts may have caused changes in HIV-1.

An alternative theory of HIV transfer to humans: oral polio vaccine

An alternative scenario for the transfer of SIV from chimpanzees to humans has been proposed: the oral polio vaccine theory. (Hooper) Approximately one million adults and children received oral polio vaccine in studies carried out in central Africa and west Africa between 1957 and 1960. (Hooper, p 730)

The polio virus used to make the vaccines used in these studies was grown in monkey kidneys. Some virus is alleged to have been grown in a solution containing chimpanzee kidneys. SIV from chimpanzees might have survived the vaccine preparation process and been transferred into humans by vaccination. A monkey virus, SV40, contaminated some polio vaccines used before 1963, suggesting that production methods could have allowed contamination of polio vaccines by viruses. (Carbone)

The chief argument supporting the oral polio vaccine theory is the fact that almost all samples of blood or tissue containing HIV from before 1981 come from places in DRC and Burundi where the oral polio vaccine was given. (Hooper, pp 740-55) Also, HIV has not been detected in any tissue samples stored before 1959 despite intensive investigations. If HIV had been present before the late 1950s, large-scale labour migration and the frequent medical use of non-sterile injections should have spread the virus more widely, advocates of the oral polio vaccine theory have argued. (Hooper, pp 676-84)

However, a study of stored oral polio vaccine samples failed to detect SIV or HIV. The study also showed that trypsin, a chemical used in the preparation of the vaccine, would kill SIV. (Garrett) Oral polio vaccine researchers have said that chimpanzee kidneys were not used in the production of vaccines. Scientists have also questioned whether enough SIV could have been transferred in the oral polio vaccine to cause infection. (Hooper, pp 647-53, 657)

Claims about the man-made origins of HIV

During the 1980s, claims circulated regarding the man-made origins of HIV. Several reports alleged that HIV was manufactured in a biological weapons laboratory at Fort Detrick in the United States in 1977 and subsequently transferred to Zaire. There is no evidence that such experiments took place. As described below, viral sequencing studies have demonstrated that HIV-1 was present in Africa and the United States before 1977.

How did HIV spread from central Africa to other parts of the world?

Studies of the evolution of HIV-1 have estimated that HIV-1 reached Haiti around 1966. (Gilbert) (Robbins) Haitians were recruited to provide technical assistance in the Democratic Republic of the Congo after independence and one case of HIV-1 subtype B infection probably established HIV-1 in Haiti. (Pépin, pp 272-3) It is possible, although not proven, that a commercial blood donation centre in Haiti’s capital amplified HIV transmission through unhygienic and unethical blood donation practices during the early 1970s. (Pépin, pp 279-284)

Numerous studies have speculated that HIV-1 subtype B passed from Haiti to the United States as a result of sex between men. The precise timing and pathways of transmission are unclear but a genetic study of HIV-1 in Haitians diagnosed with AIDS in the United States concluded that the chance that HIV-1 arrived in Haiti from the United States, rather than the other way round, was miniscule. (Gilbert)

A possible case of AIDS in the United States occurred in 1968. A young Black man died of disseminated Kaposi's sarcoma, an AIDS-defining cancer. Western blot testing of stored samples revealed HIV-1 subtype B infection. (Grmek; Garry)

HIV-1 began to spread in North American populations in the mid-1970s. The earliest evidence of HIV found in stored samples from the 1970s includes:

• Stored blood samples taken in 1978 show that 4% of gay men in San Francisco and 6% of gay men in New York taking part in a study of a hepatitis B vaccine had HIV. (Jaffe) (Stevens)
• Six cases of perinatal HIV infection were diagnosed in infants born to women who injected drugs in New York in 1977. (Thomas)
• HIV was detected in stored blood samples taken from people with haemophilia in 1978. (Evatt) Factor VIII concentrates, which provided the clotting factor missing in haemophilia, were manufactured by harvesting Factor VIII from up to 25,000 plasma donors at a time.

The United States was the source of multiple HIV-1 subtype B introductions into Europe during the 1980s, through sex between men, contaminated Factor VIII, and shared injecting equipment.

AIDS identified in 1981

The first cases of AIDS were identified among gay men in the United States in 1981. (Centers for Disease Control and Prevention) Subsequent investigations have found probable cases in adults and children dating back to 1978, supporting the view that HIV began to circulate in the United States in the 1970s.

A family in Norway died of AIDS in 1976 and stored blood samples show that the father had acquired HIV-1 type O while in Africa in 1961. (Froland)

In Haiti, probable cases of AIDS were identified in 1978 and 1979. The number of cases began to grow from 1980 onwards, and cases of AIDS were also diagnosed in Haitians who had emigrated to the United States and Canada. (Pape) (Laverdiere)

In Africa, a disease known locally as ‘Slim’ began to appear in the Rakai district of Uganda and the neighbouring district of Kagera in Tanzania in 1980. (Hooper, pp 38-42) In Zaire (now DRC), illnesses subsequently recognised as AIDS-related were recorded by hospitals in Kinshasa from 1975 onwards. (Piot) A retrospective study of mothers who gave birth in Kinshasa in 1980 found that 3% were HIV positive. (Desmyter)