We also show that AIDS has likely afflicted chimpanzees long before the emergence of HIV.
Tracing the genetic changes that occurred as SIVs crossed from monkeys to apes and from apes to humans provides a new framework to examine the requirements of successful host switches and to gauge future zoonotic risk. HIV-1 spreads by sexual, percutaneous, and perinatal routes (Hladik and Mc Elrath 2008; Cohen et al.
2010), and it is tempting to speculate that less ubiquitous SIVs were acquired more recently and/or may be more pathogenic.
Of the many primate lentiviruses that have been identified, SIVcpz has been of particular interest because of its close genetic relationship to HIV-1 (Fig. However, studies of this virus have proven to be challenging because of the endangered status of chimpanzees.
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.
The park is home to three communities, termed Kasekela, Mitumba, and Kalande, which have been studied by Goodall and colleagues since the 1960s, 1980s, and 1990s, respectively (Pusey et al. Prospective studies of SIVcpz in Gombe began in 2000 (Santiago et al. By 2009, infections were documented in all three communities, with mean biannual prevalence rates of 13%, 12%, and 46% in Mitumba, Kasekela, and Kalande, respectively (Rudicell et al. Analysis of epidemiologically linked infections revealed that SIVcpz spreads primarily through sexual routes, with an estimated transmission probability per coital act (0.0008–0.0015) that is similar to that of HIV-1 among heterosexual humans (0.0011) (Gray et al. Age-corrected mortality analyses revealed that infected chimpanzees had a 10- to 16-fold increased risk of death compared to uninfected chimpanzees (Keele et al. SIVcpz-infected females were less likely to give birth and had a much higher infant mortality rate than uninfected females.
Postmortem analyses revealed significant CD4 T-cell depletion in three infected individuals, but not in either of two uninfected individuals.
Both HIVs are the result of multiple cross-species transmissions of simian immunodeficiency viruses (SIVs) naturally infecting African primates.
Most of these transfers resulted in viruses that spread in humans to only a limited extent.
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 (
A retrovirus, now termed human immunodeficiency virus type 1 (HIV-1), was subsequently identified as the causative agent of what has since become one of the most devastating infectious diseases to have emerged in recent history (Barre-Sinoussi et al. Although antiretroviral treatment has reduced the toll of AIDS- related deaths, access to therapy is not universal, and the prospects of curative treatments and an effective vaccine are uncertain (Barouch 2008; Richman et al. Thus, AIDS will continue to pose a significant public health threat for decades to come. These relationships provided the first evidence that AIDS had emerged in both humans and macaques as a consequence of cross-species infections with lentiviruses from different primate species (Sharp et al. Indeed, subsequent studies confirmed that SIVmac was not a natural pathogen of macaques (which are Asian primates), but had been generated inadvertently in US primate centers by inoculating various species of macaques with blood and/or tissues from naturally infected sooty mangabeys (Apetrei et al. Similarly, it became clear that HIV-1 and HIV-2 were the result of zoonotic transfers of viruses infecting primates in Africa (Hahn et al. In this article, we summarize what is known about the simian precursors of HIV-1 and HIV-2, and retrace the steps that led to the AIDS pandemic. Old World monkeys are naturally infected with more than 40 different lentiviruses, termed simian immunodeficiency viruses (SIVs) with a suffix to denote their primate species of origin (e.g., SIVsmm from sooty mangabeys).
That is, viral sequences from members of the same species form a monophyletic clade in evolutionary trees.