Emerging infectious diseases (EIDs) are a major threat to human health and in recent decades we observed the rise in new epidemics in the human population. Importantly, the majority of EID events (60.3%) are caused by zoonotic pathogens and more than 70% have their origin in wildlife . AIDS is one of the most threatening infectious diseases with a zoonotic origin to have emerged in the twentieth century. Simian immunodeficiency viruses (SIVs) from chimpanzees and gorillas from west central Africa have crossed the species barrier on at least four occasions, leading to HIV-1 group M, N, O and P in humans [2–6]. HIV-2 group A–H result from at least eight independent transmissions of SIVs infecting sooty mangabeys from west Africa [3,7,8]. These HIV variants have different epidemiological histories and only one, HIV-1 group M, has spread worldwide, with a cumulative number of almost 60 million infections worldwide , since the description of the first AIDS cases in the 1980s . Nonhuman primates (NHPs) are also infected with other retroviruses, notably simian T-cell lymphotropic viruses (STLVs), which crossed the species barrier on multiple occasions causing human T-cell lymphotrophic virus (HTLV) infections affecting between 10 and 20 million people around the world. However, only 5% of the HTLV-infected population develops serious health problems . The simian foamy virus (SFV) is ubiquitous among NHPs and seems to infect humans without any consequence for their health [12,13]. Transmission from human to human has not been reported, but this virus represents a valuable tool to determine whether a population is exposed to potentially more dangerous pathogens hosted by NHP. The HIV-1 group M epidemic illustrates the extraordinary impact and consequences, resulting from a single zoonotic transmission. Therefore, it is important to evaluate which retroviruses the human population is exposed to and to better understand how these viruses enter, infect, adapt and spread to its new host. We review here the actual knowledge on retroviral infections in wild NHP and describe some of the factors playing a role in the transmission and emergence of such infections in the human population.
The simian retroviruses: molecular epidemiology, phylogeny and geographical distribution
This review will focus on three simian retroviruses: SIV, STLV and SFV.
Simian immunodeficiency viruses
Evolution and phylogeny of simian immunodeficiency viruses
To date, 45 species of NHPs among the 73 recognized species from Africa showed serological evidence of SIV infection, and in the majority of them, SIV has been confirmed by viral sequence analysis (Table 1) [14–29]. Up to 90% of the NHP species tested were SIV-positive; therefore, we can speculate that, among the remaining approximately 30 species to investigate, the majority could show a positive profile. Interestingly, SIV infection has not been documented in Asian or South American NHPs, although no large surveys have been conducted yet on wild NHP species in these continents. The genetic diversity of NHP lentiviruses is extremely complex and, although each species is infected with a species-specific SIV (Fig. 1), the SIV phylogenetic clusters are only partially superimposable on trees representing phylogenetic relations between NHP hosts. On one hand, there are profiles suggesting correspondence between virus and host phylogeny, as for SIVs infecting the four African green monkey subspecies (Chlorocebus spp.) or SIVs infecting arboreal Cercopithecus species [30,31]. On the other hand, there are SIV phylogenetic trees matching with several NHP species profiles, demonstrating the possibility of cross-species transmissions of SIVs between NHP sharing the same habitat. For example, SIVagm infecting African green monkeys has been transmitted to Patas monkeys in west Africa  and to baboons in south Africa . Cross-species transmission followed by recombination between different SIV strains can also occur among NHP species sharing the same habitat, as demonstrated for SIVmus-2 infecting mustached monkeys from Cameroon. This is a virus issued from the recombination between SIVgsn infecting greater spot-nosed monkeys and SIVmus infecting mustached monkeys . SIVcpz infecting chimpanzees is another example of cross-species transmission, followed by recombination between SIVrcm from red-capped mangabeys and SIVgsn from the greater spot-nosed monkeys’ lineage . Chimpanzees were most probably infected with these viruses, while hunting and consuming the monkey flesh. The recombination must have occurred within a chimpanzee and the new virus became the common ancestor of today's SIVcpz lineages, which was subsequently transmitted to gorillas and humans . A single NHP species can also be infected with two different viruses, as in the case of SIVmus-1 and SIVmus-2 in mustached monkeys  or, depending on the geographic region the species occupies, as for mandrills, which are infected with SIVmnd-1 south of the Ogooue River and SIVmnd-2 north of the river in Gabon and in Cameroon .
Simian immunodeficiency virus molecular epidemiology, prevalence and diagnostic techniques
Despite the fact that SIVs have been identified in 45 different NHP species from Africa, information on prevalence and molecular epidemiology are lacking for most of them (Table 1). The challenge of studying SIV infection in wild NHPs relies on the fact that these endangered populations live in remote forest regions and are difficult to spot and follow. At first, SIV infection tests were conducted using blood drawn from captive animals, either living in zoos, primate centers or kept as pets. Therefore, results on SIV prevalence were far from reflecting the situation of the populations in the wild. It was, thus, important to develop a noninvasive approach and significant efforts have been made to optimize the detection of antibodies and viral RNA in fecal samples, although at lower sensitivities than in blood .
Large-scale molecular epidemiological studies were initiated across Africa with this approach, and several thousand fecal samples were collected from chimpanzees to investigate more in detail the origin of HIV-1. These studies revealed a prevalence ranging from 0 up to 35% of SIVcpzPtt and SIVcpzPts in Pan troglodytes troglodytes from west central Africa and in Pan troglodytes schweinfurthii from east Africa [4,38,39]. These studies also showed that SIVcpzPtt strains are significantly more closely related to HIV-1 strains from humans, and that the ancestors of HIV-1 M and N could be traced to distinct chimpanzee communities in south-east and south-central Cameroon . Despite testing of numerous samples, no SIV infection has been detected yet in the other two chimpanzee subspecies, Pan troglodytes ellioti (previously Pan troglodytes vellerosus) and Pan troglodytes verus[4,40–42] (Fig. 2). Another large molecular epidemiological survey, aimed at studying the origins of HIV-1, was conducted across southern Cameroon on fecal samples from wild gorillas. Gorillas are infected with SIVgor and this study showed that the overall SIVgor prevalence was three times smaller than that observed in chimpanzees in the same areas. SIVgor strains form a monophyletic group within the HIV-1/SIVcpzPtt radiation, but they are all most closely related to the HIV-1 O and P groups [5,6,43]. HIV-1 P is most likely of gorilla origin, but the reservoirs of the direct ancestors of HIV-1 O have not been identified yet. The four HIV-1 groups fall within the HIV-1/SIVcpzPtt/SIVgor radiation; therefore, the cross-species transmissions giving rise to HIV-1 occurred most likely in western equatorial Africa, home of P.t. troglodytes chimpanzees and western lowland gorillas (Gorilla gorilla gorilla) (Fig. 2). Noninvasive surveys were also conducted among wild NHP populations in Côte d’Ivoire and the ancestors of the HIV-2 group A and B viruses, responsible for the HIV-2 epidemic in west Africa, were identified in wild sooty mangabey populations in the Tai forest in Côte d’Ivoire, close to the border with Liberia . In general, the knowledge on SIV prevalence and geographic distribution remains limited today, because only a few large-scale studies have been conducted on retroviral infections in wild primate populations. Collecting and analyzing fecal samples is difficult, very labor-intensive in the field and also in the laboratory. It becomes even more challenging when arboreal species are investigated, as illustrated by studies on Colobinae and Cercopithecus species from the Tai forest in Côte d’Ivoire. Moreover, if antibody detection is not possible in fecal samples, as in some Colobus species, screening by viral RNA amplification is necessary [45,46].
An alternative approach to determine the SIV prevalence, and, indirectly, to measure simultaneously the extent of SIV exposure in the human population, is to analyze tissue and/or blood samples collected from NHP bushmeat. The bushmeat trade contributes to the decline of many endangered primate species and it is, therefore, important not to encourage further hunting while collecting samples at the markets. Studies on bushmeat samples from different forest regions in Cameroon and in the Democratic Republic of Congo (DRC) revealed an overall SIV seroprevalence of 3 and 19%, respectively. These studies also showed significantly different prevalence rates per species (0 to >40%), and variations within species according to the sampling site [18,19].
Estimating the SIV prevalence in wild living NHP populations also requires considering the relative specificity and sensitivity of the serological tests available. Early studies relied on HIV screening or confirmatory assays, which are based on cross-reactivity with HIV-1 and/or HIV-2 antigens, which could underestimate the SIV prevalence. Further on, immuno-enzymatic methods (i.e. ELISA) have been developed, targeting specific SIV lineages, to increase the tests sensitivity [18,47–49]. Meanwhile, the number of new SIV lineages as well as the genetic diversity within lineages has increased; therefore, the number of antigens, which needed to be included in the tests, became important. To contain the workload and to limit the amount of biological material, often available at very low quantities, a multiple analyte profiling technology (xMAP) has been adapted to allow a single sample to be tested simultaneously for 35 peptides with similar sensitivities and specificities .
Transmission and pathogenicity of simian immunodeficiency virus in the natural host
There is still little information available today on SIV pathogenic properties and on the transmission routes in its natural host. Horizontal transmission by sexual contact or biting, and vertical transmission, has been demonstrated [36,44,50–53].
On the basis of studies on SIVagm and SIVsmm infections in captive African green monkeys and sooty mangabeys , and despite active viral replication and high-prevalence levels, SIV infections were until very recently, generally considered nonpathogenic in their natural hosts [55–57]. Progression to AIDS has been observed in a few captive NHP, who lived past the average life span and were infected over long periods. Two mandrills infected with SIVmnd-1 and SIVmnd-2 developed AIDS, after 17 years of SIV infection ; a sooty mangabey naturally infected with SIVsmm progressed to AIDS after 18 years and an African green monkey co-infected with SIVagm and STLV was also reported to progress to AIDS [59,60]. The general assumption that all natural SIV infections were harmless has been challenged recently by a study conducted on two habituated populations of chimpanzees (P.t. schweinfurthii) at Gombe National Park in Tanzania. The SIV infectious status was assessed, by analyzing the fecal samples collected on a regular basis for more than 10 years. SIV infection was associated with a 10–16-fold increase in age-corrected risk of death. Fertility was significantly reduced in SIV-positive females, both in terms of their birth rate and the survival of the offspring. Immunohistochemistry and in-situ hybridization of postmortem spleen and lymph node samples showed lower CD4+ T-cell counts in SIV-positive versus SIV-negative individuals. CD4+ T-cell counts and tissue samples strongly resembled the histopathology of human end-stage AIDS patients . Similarly, a recent report on a naturally SIV-infected P.t.troglodytes chimpanzee confiscated in Cameroon in 2003, subspecies in which the ancestors of HIV-1 have been documented, also suggests clinical progression to an AIDS-like disease .
Simian T-lymphotrophic viruses
Evolution and phylogeny
To date, simian counterparts, STLV-1–3, have been described for HTLV type 1–3 in humans, and no simian virus analogue to the recently discovered HTLV-4 has been identified yet . Conversely, no human analogue has been reported today for the tentatively identified STLV-5 in a macaque species from Asia . Since the first descriptions of STLV and HTLV around 1980 , the virus has infected between 10 and 20 million people worldwide. In contrast to HIV, the majority of HTLV-1 infections remain asymptomatic: about 5% of them are associated with severe diseases, such as adult T-cell leukemia/lymphoma, or inflammatory diseases of the central nervous system, such as the HTLV-1-associated myelopathy/tropical spastic paraparesis [11,65]. HTLV-2 is less pathogenic  and no information is available yet for the recently described HTLV-3 and HTLV-4, but viral structure of HTLV-3 suggests a pathogenic potential similar to HTLV- 1 [67,68].
Simian T-lymphotrophic virus molecular epidemiology, prevalence and diagnostic techniques
Although STLV-1 has been documented in more than 30 Old World monkey species and apes from sub-Saharan Africa and Asia, STLV-3 has only been isolated in African monkeys and STLV-2 only in bonobos, an ape species endemic to DRC [20,69–71] (Table 1). Phylogenetic analyses show that STLV-1 and STLV-3 cluster by geography, rather than by host species, and STLV-1 and STLV-3 viruses are interspersed within the different HTLV-1 and HTLV-3 subtypes, suggesting not only multiple cross-species transmissions among NHPs but also from NHPs to humans (Fig. 3a and b) [20,71–75]. Cocirculation of STLV-1 and STLV-3 within the same species, in the same geographic area, has been documented, as well from different STLV-1 and/or STLV-3 subtypes [20–22].
As observed for SIV, prevalence varied according to the species investigated, ranging between 0.0 and 80% [20,23,76]. Eight to 11% of NHP bushmeat samples from Cameroon and DRC, respectively, are infected with STLV [20,22]. Most of the STLV-infected NHPs display a serological profile very close to that observed in humans infected with HTLV, but it is not known to what extent divergent strains cross-react with the antigens currently used. Similarly, STLV prevalence and genetic diversity can be underestimated for the same reasons described for SIV.
Transmission and pathogenicity of simian T-lymphotrophic virus in the natural host
STLV infection within the same species occurs mainly through sexual contact, aggressive behavior and breastfeeding [77–79]. Aggressive behavior and hunting sympatric STLV-infected species seems to be the most plausible route for STLV cross-species transmission [79–81]. STLV-1 has occasionally been associated with malignant lymphoma or leukemia in macaques, baboons, African green monkeys and gorillas [82–88]. A case of STLV-1 transmission between captive heterologous species (from rhesus macaques to baboons) enhanced oncogenicity in the infected animal, whereas this phenomenon was not observed between homologous macaque species residing in the same center .
Simian foamy viruses
SFVs are ubiquitous in NHPs and have been identified in a wide variety of primates, including Prosimians, New World and Old World monkeys as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV . SFVs are ancient and well adapted viruses that have co-evolved with their NHPs hosts for more than 30 million years . Little is known about the prevalence and transmission patterns of SFV in wild-living primate populations. SFVs are highly prevalent in captive primate populations, with infection rates ranging from 70 to 100% in adult animals [90–93], and free-ranging macaques from Indonesia , Thailand, Nepal and Singapore . Recently, using a fecal-based assay, a high SFV infection rate (44–100%) was detected in chimpanzees from west, central and east Africa. Remarkably, all of the 120 newly characterized SFVcpz strains clustered according to their subspecies of origin .
The saliva and blood of infected animals are considered the principal routes of SFV transmission [97,98], but SFVcpz sequences were also found in every targeted body compartment of two chimpanzees examined postmortem . Studies in chimpanzees and African green monkeys indicate predominantly horizontal rather than vertical transmission routes [96,97].
There is no human foamy virus, but SFV infections have been reported in persons occupationally exposed to NHPs and in a few hunters in central Africa with no consequence for their health [100–104]. Efficient transmission of SFVs after ape bites, followed by viral persistence, has been reported in central African hunters [104–106]. No SFV epidemic has been documented yet, and the lack of human-to-human SFV transmission represents an informative marker of contact between human and NHPs.
Simian retroviruses: factors and conditions necessary for a successful transmission to humans
Although the conditions and circumstances determining SIV, STLV and SFV transmission from NHPs to humans are not completely elucidated, exposure to blood or other secretions of infected animals, through hunting and butchering of bushmeat, or through bites and scratches inflicted by pet NHPs, represent the most plausible source for human infection (Fig. 4). Direct evidence for such events has been reported recently for STLV and SFV in primate hunters in independent studies in Cameroon and Gabon [101,104,106–108]. SIV antibodies have been detected in humans exposed to NHP, but the viruses could not be amplified by molecular techniques, suggesting only exposure but no replication [36,109]. Persistent presence of antibodies without detectable viral nucleic acids has also been previously observed in a laboratory worker who has been accidentally exposed to blood from a SIV-infected macaque .
Factors associated with single cross-species transmission have to be differentiated from those associated with epidemic spread, the latter being a combination of multiple factors. For an animal pathogen to become successful in humans, it must evolve into a pathogen capable of not only infecting humans but of also maintaining long-term human-to-human transmission without the need for re-introduction from the original animal host. Several steps are, thus, necessary for a disease of zoonotic origin to become a pandemic, a topic extensively discussed in several reviews [111,112]. The type and intensity of contacts between the reservoir host (donor) or its viruses and the new host (recipient), the host barrier to infection at the organism or cell level, the viral factors allowing efficient infection in the new host and the determinants of efficient virus spread within the new host population are all factors that mediate the transition from one stage to the next.
Exposure to simian retroviruses
The chance for cross-species transmissions could increase when frequency of exposure and retrovirus prevalence is high. According to the most recent data, human exposure to SIV or STLV appears heterogeneous across the African countries surveyed [18,19,22,76]. For example, SIV prevalence in NHP bushmeat in Cameroon and DRC is 3 and 19%, respectively, but infection rates can vary significantly according to the species tested (0–50%) [18,19]. Interestingly, in Cameroon the lowest prevalence (0–1%) was observed among the most frequently hunted species (>90% of NHP bushmeat). On the contrary, in DRC, the highest prevalence (25%) was reported in the most frequently hunted monkeys (Fig. 5) [18,19]. In wild-living chimpanzee and sooty mangabey populations in which the HIV-1 M, N and HIV-2 A and B ancestors have been described, SIVcpz and SIVsmm prevalence have been measured at about 30 and 50% [4,42,44], respectively, but this is not sufficient to explain why these viruses became the ancestors of HIV-1 group M and HIV-2 group A and B epidemics. This is illustrated by a study reporting a high prevalence of SIVsmm in feral sooty mangabeys in which viruses were closely related to HIV-2 strains described in isolated human cases in rural Sierra Leone and Liberia .
Although studies showed that humans in central Africa are exposed to blood and body fluids from a wide variety of NHP species [18,19,101,114], we generally lack data on prevalence in wild-living primates. Given the number of species infected, cross-species transmissions of other retroviruses to humans should be considered. The recently documented transmissions of SFV and STLV highlight the risk for potential emergence of a new SIV into the human population [101,103–105,107,108]. The description in 2009 of HIV-1 group P , closely related to SIVgor, in a Cameroonian patient living in France, shows clearly that our knowledge on HIV diversity and possible cross-species transmissions is still incomplete and illustrates how rapidly new viruses can spread today to other continents.
After exposure and direct contact, the second step for the pathogen to be able to infect the new host is for pathogen and host to be ‘compatible’. Crucial to the ability of a virus to infect hosts is the presence of appropriate receptors on host cells. When receptors are conserved across a range of possible host species, the hosts are likely to be predisposed to infection by viruses using these receptors. SIVwrc infecting western red colobus provides an example on the importance of viral adaptation and host factors in determining a successful cross-species transmission. Overall, 50–80% of them are infected with SIVs [23,45] and, together with mangabeys, they are heavily hunted for bushmeat . However, in contrast to SIVsmm, no SIVwrc cross-species transmission to humans has been documented yet. Moreover, western red colobus represent 80% of animal proteins ingested by the chimpanzee subspecies (P.t.verus) living in the Tai forest in Côte d’Ivoire , but no SIVwrc infection could be identified in its predator .
Our knowledge on the role of viral and host factors to efficiently infect and adapt to a new host are still incomplete and they are most probably very complex. Several retroviral restriction factors have been identified in humans, APOBEC3G induces lethal hyper mutations in the retroviral genome, Trim5α proteins restrict the incoming viral capsid, tetherin inhibits the release of viral particles (reviewed in ) and SAMHD1 is an antiretroviral protein expressed in cells of the myeloid lineage that inhibits an early step of the viral lifecycle . Primate lentiviruses have acquired accessory genes that can antagonize these antiviral host restriction factors: for example, the Vpu protein of the pandemic HIV-1 M strain is able to block the human restriction factor tetherin, whereas HIV-1 O viruses do not . As a consequence, this could have led to a higher replication of HIV-1 M in humans, a better human-to-human transmission and a better epidemic spread of HIV-1 M versus O in the human population [118,121]. The higher pathogenicity of HIV-1 can also be partially explained by the fact that the function of nef, that allows viral persistence in the host while controlling for superactivation of the immune system, is lost in certain SIV lineages and, more precisely, in the ancestors of the HIV-1/SIVcpz lineage in contrast to SIVsmm/HIV-2, where this adaptation is not observed and where the virus is less pathogenic [122,123]. An adaptation of SIVcpz to its new host has been proposed at the Gag-30 position in the p17 region of the gag gene, in which methionine or leucine is present among SIVcpz/SIVgor, whereas all HIV-1 strains harbor an arginine at this position . The lower viral fitness of HIV-2 compared with HIV-1, and of HIV-1 O versus M, could also partially explain the lower prevalence and limited spread of HIV-2 and HIV-1 O . In general, the frequent examples of cross-species transmissions of SIVs and STLVs among NHPs illustrate that retroviruses have the potential to easily adapt to a new host. Moreover, many SIV lineages have the ability to replicate in vitro in human lymphocytes [126–135]. Although important progress has been made to understand the complex interactions between lentiviruses and their host, more comparative studies of humans, NHP and their respective viruses are needed.
Epidemic spread in the new host species
The next step in a successful species jump for the pathogen is to be sufficiently transmissible among individuals within the new host population. To become fully established, HIV likely required also changes in human behavior. The combination between increasing human density in forest areas, urbanization and human migration from rural to urban areas facilitated the spread. Commercial sex and traditional and new medicinal practices were promoting efficient transmission [136–138]. Iatrogenic factors, that is, the use of unsterilized needles in parenteral mass treatment of certain tropical diseases such as sleeping sickness or syphilis may have been responsible for the start of the HIV pandemic from a few isolated cases of infection to a larger reservoir, allowing subsequent sustained human-to-human sexual transmission of HIV . In addition, serial passages of partially adapted SIVs among humans could have produced a series of cumulative mutations sufficient for the emergence of the epidemic HIV strains [136,137]. Also in the USA and Europe, the initial HIV spillover was observed among populations adopting high-risk sexual behavior or IDUs and among people receiving multiple blood transfusions. The presence of sexually transmitted diseases inducing genital ulcers such as herpes simplex virus type 2 enhance the risk of acquiring HIV infection  and probably played a role in efficient sexual spread in the early twentieth century . Conversely, male circumcision seems to limit the chance of contracting HIV [142–144]. The combination of some or all of these factors may have contributed more or less effectively to the spread of the virus in certain population groups and geographic areas.
The first AIDS cases have been described around 1980 in the USA , but the virus circulated already early in the twentieth century in the human population in central Africa. It has been estimated by molecular clock analysis that the most recent common ancestor of HIV-1 group M exists since about 1908, and two viruses obtained from blood and tissue samples collected in 1959 and 1960 in Kinshasa indicate that HIV-1 M was already spreading among humans in central Africa 20 years before the recognition of the AIDS epidemic [145,146]. Chimpanzees have been hunted for hundred years in central Africa, and SIVcpz, SIVsmm, STLVs or other retroviral cross-species transmissions most likely occurred at multiple occasions. The fact that the HIV-1 M ancestor was isolated in chimpanzees living in south Cameroon, and that the origin of the epidemic was recorded in Kinshasa, the capital city of DRC , located at over a thousand kilometers from the HIV-1 M reservoir, highlights the importance of the role of human factors in the epidemic spread. The development of major cities, such as Kinshasa, in Africa, occurred also in the twentieth century  and provided most likely an ideal new socio-economic environment, allowing epidemic spread of a sexually transmitted and blood-borne pathogenic agent (Fig. 6).
Simian retroviruses cross-species transmission in the socio-economic context of the twenty-first century
NHPs have been hunted in west and central Africa for millennia and today many people, especially in rural areas, still rely on bushmeat for subsistence. Unfortunately, hunting has shifted to an organized activity, commercial venture, with eruption of the bushmeat crisis in the late 1980s and early 1990s in the Congo Basin [149,150]. Growing urban populations have commercialized the trade and, in the Congo Basin alone, harvest estimates for all species combined range from 1 to 3.4 million metric tons per year [151–154]. The transportation infrastructure between rural and urban areas provided by the logging industry increased exponentially during the second part of the twentieth century  and brought roads, trucks, guns and workers with their families into forest areas once far less accessible . The expansion of oil and mining industries also participated in attracting human population to live in tropical forests. Humans are, thus, more and more exposed to simian retroviruses and other pathogens. Armed conflicts also contributed to the increase in the bushmeat trade  and led to profound socio-economic changes and internal displacement of human populations . Importantly, high HIV prevalence was reported around logging industries and in displaced population groups [158,159]. In contrast to the early twentieth century, more people with immune deficiency are now exposed to new pathogens, and superinfection with a new SIV could lead to the recombination between HIVs and SIVs, allowing for a potentially more efficient adaptation and replication in the new host. Importantly, cross-species transmissions from NHPs to humans will most likely occur in rural areas, where, even today, access to health services is poor . This means that new epidemic outbreaks, especially regarding diseases with a long incubation period, can still go unrecognized for a long time. In addition, these SIV strains are not recognized by commercial HIV-1/HIV-2 screening assays. Compared with the early twentieth century, travelling between urban and rural areas has significantly increased, and viruses nowadays can reach rapidly new areas with favorable conditions for epidemic spread. In addition, air travel allows pathogens to cross nations and even continents fast, challenging further the ability to control the emergence of diseases.
Prevalence and exposure are among the variables playing a role in the transmission of simian retroviruses to humans, but viral and host molecular characteristics are fundamental factors to establish efficient infection and disease. Given the ongoing and increasing contact between NHP and African populations through hunting and butchering, it is likely that SIV and other simian viruses are still transmitted to humans. Travelling is on the rise, and new viruses can rapidly reach new areas with favorable conditions for epidemic spread. By improving our knowledge about the NHP retroviral reservoir, we will be able to update, adapt and improve the current diagnostic tools. The development of new high-throughput serological and molecular assays, able to identify a wide diversity of simian retroviruses, will allow large-scale studies at the human–primate interface in areas of Africa where the emergence of new zoonotic diseases is likely to occur. By adding the expertise and support of disciplines such as healthcare, social sciences, primatology, biodiversity, economy and mathematics, it will be possible to target better and faster new cross-species transmission hotspots. It will also be important to build a network of high-quality technical and human resources, supporting detection, identification and monitoring of infectious disease, and to ensure that surveillance is linked operationally to an appropriate response.
The authors thank Eric Delaporte for comments on an early version of the manuscript and Mary K. Gonder for the chimpanzee distribution map. Photographs in Figure 4 were kindly provided by Sabrina Locatelli (a, b), Bernadette Abela (c), and Steve Ahuka-Mundeke (d).
S.L. and M.P. wrote the article.
Conflicts of interest
The authors declare they have no conflicts of interest.
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