The real grounds for believing that the dominant form of the virus originated in western equatorial Africa, probably in the broad area of Cameroun and the Democratic Republic of Congo (DR Congo), lie in three other directions. One is that HIV clearly results from the transmission to human beings of the ancient and related simian immunodeficiency virus (SIV), an infection of African monkeys that had also spread to chimpanzees.4 That such an animal disease should pass to humans is not surprising, because several major human infectious diseases are contracted from animals, notably plague, sleeping sickness, yellow fever, some forms of influenza, and, most recently, Creutzfeldt-Jakob’s Disease.5 How such a transmission took place with HIV will never be known, but one possibility may have been infection by blood in the course of hunting as men penetrated the equatorial forest. One study of 1,099 people engaged in hunting and butchering in Cameroun, published in 2004, found ten who had contracted simian viruses, although in this case not HIV.6 Aids is a by-product of the human mastering of the natural environment that has been the core of African history.
SIV has been transmitted from animals to humans at least eleven times and probably many more. There are two forms of the human disease: HIV-1, which is responsible for the global Aids epidemic, and HIV-2, which is less virulent and infectious and is virtually confined to the West African coast between Senegal and Côte d’Ivoire. HIV-2, discussed in Chapter 6, is closely related to the SIV common in the sooty mangabey monkeys of that region. By 2005, HIV-2 infections had been divided into eight groups, each believed to have resulted from a separate transmission. Only two of these groups, lettered A and B, had established themselves as human epidemics, suggesting that many unsuccessful transmissions may also have taken place in the past.7 By contrast, the animal virus most similar to (although still quite distant from) HIV-1 and probably ancestral to it is the SIV occasionally harboured by a species of chimpanzee (Pan troglodytes troglodytes) whose natural territory is the forest of Gabon, Equatorial Guinea, Central African Republic, Cameroun, and Congo-Brazzaville, somewhat north of Kinshasa. Three groups of HIV-1 have been identified and lettered M, N, and O. Each group must result from a separate transmission of SIV, because on a family tree of the virus they are separated by intervening SIV strains. Group M is responsible for the global epidemic that by 2005 had infected about 60 million people. Group O is equally virulent and may be at least equally old, having infected the Norwegian seaman during the 1960s, but it remained largely confined to the vicinity of Cameroun, even there causing fewer than 10 per cent of HIV cases in the early 2000s. Group N was probably a later transmission and remained very rare; in 2005 only seven cases were known, all in Cameroun.8
The fact that the likely viral ancestor of HIV-1 has been found only in the chimpanzees of western equatorial Africa is one of the three reasons for thinking that the virus originated there. The second reason is that only that region harboured not only all three groups of HIV-1 but all the subgroups of the dominant group M.9 The significance of this point arises from the nature of the virus.10 The human immunodeficiency virus is almost inconceivably small: one ten-thousandth of a millimetre in diameter. It consists of a package of genetic information (a genome) surrounded by a protein envelope, the whole containing nine genes, whereas a human being has 30,000–40,000. Like all viruses, HIV has no life of its own but is a parasite of cells, drawing its life from theirs. Transmitted from one body to another by blood, genital fluids, or human milk, the virus becomes attached to certain types of cells, the most important being the CD4 helper T-cells that activate the body’s immune system. The virus enters a cell and integrates its genetic information into its host’s, using the cell’s life to reproduce itself, which is the sole function of a virus. In doing so the virus destroys the host cell – and hence ultimately the immune system – while producing an immense number of new viruses to attack further cells. The process from entry into a cell to the production of new viruses takes on average about two days, so that HIV passes through some 180 generations a year. Moreover, the reproduction process is prone to error, because HIV’s genetic information is in the form of RNA (ribonucleic acid) and must be converted into the DNA (deoxiribonucleic acid) composing the cell’s genome. The combination of speed and error in reproduction means that HIV mutates at about 1 per cent per year, or a million times faster than is normal in evolution.11
One consequence of this rapid mutation was that when the M group of HIV-1 was analysed during the 1980s and 1990s, it displayed great diversity. Using a range of specimens from Africa, North America, and Europe, researchers identified ten subgroups that differed from one another in their composition by up to 30 per cent. They were lettered A, B, C, D, F1, F2, G, H, J, and K.12 All subgroups were found only in western equatorial Africa, although it may be more accurate to say that the fullest range of diversity existed only there, because the viruses identified in the DR Congo, in particular, show as much diversity within supposed subgroups as between them. This suggests that HIV group M evolved and diversified in the broad Congo region before certain strains were carried elsewhere to create differentiated subgroups by what is called a founder effect.13 At all events, there is a fundamental distinction between the great diversity of strains in western equatorial Africa and the domination of one or two subgroups (sometimes in combination) in every other region of the world: A and D in eastern Africa; a combination of A and G in West Africa; B in Europe and North America; C in southern Africa, Ethiopia, and India.14
Unlike many other viruses, such as influenza, HIV strains do not supplant one another at intervals but evolve and differentiate as they pass from one human body to another. Modern medical science can distinguish in great detail between these strains and reconstruct their genetic relationships. This makes it possible to write a history of HIV and its epidemic dispersal in a way that may be impossible for any other disease, using evidence from stored blood and living bodies. The first part of this book outlines such a history for the African continent. Moreover, medical science holds out at least the possibility of dating this history. It is plausible to argue that HIV mutates so extensively that its overall mutation is at a regular speed, which can be calculated from the evolutionary distance between classified specimens taken at known dates. This ‘molecular clock’ can then suggest dates for major events in the evolutionary sequence, such as the separation of one subgroup from another. One such calculation from 144 dated specimens was published in 2000, using massive computing capacity at Los Alamos. It suggested that the last common ancestor of HIV-1 group M – the point at which the subgroups of the global epidemic began to differentiate – lay around the year 1931, and with more confidence between 1915 and 1941. Since the researchers knew that the genes composing the HIV genome mutate at different speeds, they compared this calculation, based on the most mutable envelope gene, with a calculation from a less mutable gene, which suggested a 1934 date. The researchers checked their procedure further by independently dating the earliest HIV specimen taken at Kinshasa in 1959, which had been identified as an early version of the D subgroup shortly after its separation from the B subgroup. The computer dated it between 1957 and 1960.15 In 2001 another research team published similar calculations based on different specimens; they dated the last common ancestor of group M to 1937 (by the envelope gene) or 1920 (by the least mutable gene). The second research team also suggested that HIV-1 group M separated from the strain of SIV ancestral to that in modern chimpanzees around 1675, or with more confidence between 1590 and 1761.16 It would be unwise at this stage to attach too much importance to this date.
Among the many uncertainties surrounding these findings, the most relevant here is whether the notion of a molecular clock is invalidated by another feature of viral evolution known as recombination. A person can be infected by more than one strain of HIV. If that occurs, viruses of different subgroups may enter the same cell and, in the process of integrating their genetic material with the host’s, may produce a new strain of virus combining elements from two or more subgroups. (SIV is subject to the same process and the original simian virus transmitted to humans as the ancestor of HIV-1 group M is itself believed to have been a recombinant form.)17 Although the strain identified in 1959 appears not to have been a recombinant, one of the earliest recovered from the DR Congo in 1976 was, and it is even possible that supposedly discrete subgroups were products of recombination at a stage so early as to be no longer identifiable.18
