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However, it has recently become clear that, on several occasions in the past, lentiviruses have infiltrated their hosts’ germlines and become endogenous, vertically transmissible, genomic loci (Fig. Examples include the rabbit endogenous lentivirus type K (RELIK), which became germ-line embedded approximately 12 million years ago (Katzourakis et al. 2009), and two prosimian endogenous lentiviruses, which independently invaded the germ-lines of both the grey mouse lemur (p SIVgml) and the fat-tailed dwarf lemur (p SIVfdl) about 4 million years ago (Gifford et al. Molecular clocks derived from extant SIV sequences suggested that ancestral SIVs existed only a few hundreds of years ago (Wertheim and Worobey 2009), but it has long been suspected that such analyses may grossly underestimate deeper evolutionary timescales (Sharp et al. Recent studies of SIV-infected monkeys on Bioko Island, Equatorial Guinea, partly substantiated this conclusion, showing that geographically isolated subspecies have been infected with the same type of SIV for at least 30,000 years and probably much longer (Worobey et al. The endogenous viruses in lemurs reveal that the span of evolutionary history of primate lentiviruses as a whole is at least two orders of magnitude greater still.Thus, it is possible that at least some SIVs, such as those infecting four closely related species of African green monkeys ( species), have coevolved with their respective hosts for an extended period of time, perhaps even before these hosts diverged from their common ancestor (Jin et al. So far, SIV infections have only been found in African monkeys and apes, and so it seems likely that primate lentiviruses emerged in Africa sometime after the splits between lineages of African and Asian Old World monkeys, which are believed to have occurred around 6–10 million years ago (Fabre et al. However, because neither Asian nor New World primates have been sampled exhaustively, the conclusion that SIVs are restricted to African primates must remain tentative, especially because none of these primate species has been examined for endogenous forms of SIV (Ylinen et al. Thus, our understanding of the evolutionary history of primate lentiviruses is still incomplete.
Acquired Immune Deficiency Syndrome (AIDS) was first recognized as a new disease in 1981 when increasing numbers of young homosexual men succumbed to unusual opportunistic infections and rare malignancies (CDC 1981; Greene 2007). 2011); however, 80% of adults acquire HIV-1 following exposure at mucosal surfaces, and AIDS is thus primarily a sexually transmitted disease (Hladik and Mc Elrath 2008; Cohen et al. Since its first identification almost three decades ago, the pandemic form of HIV-1, also called the main (M) group, has infected at least 60 million people and caused more than 25 million deaths (Merson et al. Developing countries have experienced the greatest HIV/AIDS morbidity and mortality, with the highest prevalence rates recorded in young adults in sub-Saharan Africa (
At select field sites, mitochondrial and microsatellite analyses of host DNA were also used to confirm sample integrity and to determine the number of tested individuals. In contrast, other SIVs, such as those of sooty mangabeys and African green monkeys, are much more widely and evenly distributed and infect their hosts at generally higher prevalence rates (Phillips-Conroy et al. Sites where SIV infections were detected are highlighted in yellow. Importantly, all of more than 30 sequenced SIVcpz strains show an identical mosaic genome structure.
Figure 3A summarizes current molecular epidemiological data derived from the analysis of over 7,000 chimpanzee fecal samples collected at nearly 90 field sites (Santiago et al. The upper panel depicts the ranges of the four subspecies of the common chimpanzee (, brown) gorillas (map courtesy of Lilian Pintea, The Jane Goodall Institute). Moreover, there is no evidence that chimpanzees harbor any other SIV, although they, as well as bonobos, are routinely exposed to SIVs through their hunting behavior (Mitani and Watts 1999; Surbeck and Hohmann 2008; Leendertz et al. Initially, SIVcpz was thought to be harmless for its natural host.
Data were compiled from several studies (Santiago et al. This was because none of the few captive apes that were naturally SIVcpz infected suffered from overt immunodeficiency, although in retrospect this conclusion was based on the immunological and virological analyses of only a single naturally infected chimpanzee (Heeney et al. In addition, SIV-infected sooty mangabeys and African green monkeys showed no sign of disease despite high viral loads in blood and lymphatic tissues (Paiardini et al.
2009), leading to the belief that all naturally occurring SIV infections are nonpathogenic.