Fig. 13.27 Phylogenetic origins of HIV-1 and HIV-2. HiV-1 shows marked genetic variability and is classified on the basis of genomic sequence into four major groups: M (main), O (outlier), n (non-M, non-O), and P (non-M, non-n, non-O), which are further diversified into subtypes, or clades, that are designated by the letters a to K. in different parts of the world, different subtypes predominate. Phylogenetic analyses of chimpanzee simian immunodeficiency virus (SiVcpz), gorilla SiV (SiVgor), and HiV-1 sequences demonstrate that the four groups of HiV-1 (M, n, O, and P) originated from four independent cross-species transmission events: two transfers of SiVcpzPtt from central chimpanzees (subspecies Pan troglodytes troglodytes, or Ptt) gave rise to HiV-1 groups M and n, while two transfers of SiVgor from western lowland gorillas (subspecies Gorilla gorilla gorilla) gave rise to HiV-1 groups O and P. Similarly, separate zoonotic transmissions of SiVsmm from sooty mangabey monkeys to humans are responsible for at least nine different lineages of HiV-2 (groups a–H and a newly described lineage, u). SiVstm and SiVmac resulted from experimental infections of stump-tailed macaques and rhesus macaques with SiVsmm, respectively. abbreviations: cpzPts, chimpanzee Pan troglodytes schweinfurthii; cpzPtt, chimpanzee Pan troglodytes troglodytes; mac, macaque; SiV, simian immunodeficiency virus; smm, sooty mangabey monkey; stm, stump-tailed macaque. Figure courtesy of  Drs. Beatrice Hahn and Gerald learn.
to humans on at least four independent occasions from chimpanzees or western lowland gorillas, whereas HIV2 originated in the sooty mangabey (Fig. 13.27). The best estimate is that the most prevalent of the four major variants of HIV1, group M (responsible for ~99% of HIV1 infections worldwide), was transmitted to humans from chimpanzees in the first half of the twentieth century; transmission of group O also dates to the early twentieth century, whereas the two other HIV1 variants (groups N and P) appear to have been transmitted more recently. As is true for other zoonotic infections where there has been insufficient time for pathogen and host to coevolve to an equilibrium that attenuates virulence, SIV is generally less pathogenic in its nonhuman primate host than is HIV in its human host. Thus, whereas development of AIDS is nearly universal in HIV1infected humans that do not receive treatment, development of AIDS in SIVinfected nonhuman primates is considerably more variable, with some primates failing to develop disease at all.