During the early stages of infant development the capacity for perceptual (i.e., visual) discrimination is shaped by infants' perceptual experience. Perceptual narrowing is one process hypothesized to account for developmental change. Perceptual narrowing research often demonstrates that infants before 6 months of age are able to discriminate a wide variety of events whereas infants beyond 6 months of age seemingly "lose" some perceptual abilities. Two investigations are proposed to examine the claim that younger, but not older infants can discriminate faces across species. The purpose of Experiment 1 was to determine whether an increase in familiarization and trial times would result in cross-species facial (i.e. faces of macaques) discrimination in 12-month-olds. The hypothesis was supported, adding evidence that perceptual discrimination becomes more constricted, or less efficient with age, but does not decline. Experiment 2 examined whether reducing both the time of familiarization and comparison time by 50% would allow infants sufficient time to discriminate. Results were consistent with the hypothesis and previous studies were corroborated. These findings highlight the important role of perceptual experience in young infants' perceptual discrimination abilities and provide a greater degree of clarity regarding present use of the concept perceptual narrowing.

Successful architecture is an engagement of space that fosters learning and growth. It is the space in which we are drawn away from the distractions around us, allowing us to focus on the present. It offers the opportunity to not only learn and grow relationships, but also to rehabilitate broken and fractured ones. Through this learning and growth, we become better understanding and loving toward each other. Thus, architecture stands as a true mediator of the relationships that exist around the world. Architecture is not exclusive toward human to human engagement. Architecture can extend beyond the understanding of human and engage many species such as canines. This thesis proposes to investigate a cross-species architecture serving to rehabilitate broken and fractured interspecies relationships. Focusing on one of the strongest human-interspecies relationships to exist, this thesis will conduct research-based design on the human and dog relationship. Although the human and dog relationship are one of the stronger cross-species relationships, there remains complex and fractured components. For example, in many aspects across homeless and stray dogs, the human and dog relationship has vii become one that is extremely broken and fractured. This thesis proposes to take an in depth look at the historical context and the present human-canine relationship and understanding how architecture can be used to grow the relationship. In allowing cross-species architecture to act the mediator in rehabilitating the fractured components of the human and dog relationship, the level of learning and growth within the human and dog relationship can reach new heights.

Les SIV infectant les chimpanzés et les gorilles sont les précurseurs des virus de l'immunodéficience humaine de type 1. Les quatre groupes du VIH-1 sont le résultat de quatre transmissions virales des grands singes à l'Homme. Des méthodes non invasives ont permis d'identifier le réservoir des VIH-1 M et N dans deux communautés de chimpanzés (Ptt) au Cameroun et de montrer que les gorilles (Ggg) sont infectés par un SIV proche des VIH-1 O et P. Si le SIVgor n'a jamais été détecté chez les chimpanzés, la phylogénie montre que les Ptt ont transmis ce virus aux gorilles. Par une méthode pluridisciplinaire, nous avons étudié les caractéristiques de l'infection SIVgor en milieu naturel. Nous avons prospecté 13 sites au Cameroun et 2 en RCA. Au total, 2120 fèces de gorilles et 442 de chimpanzés ont été collectées. L'infection SIVgor a été détectée dans 3 sites Camerounais et les prévalences varient entre 3,2% et 4,6%, résultats plus faibles que ceux retrouvés chez les chimpanzés. Nous avons ensuite montré que plusieurs groupes sociaux de Ggg dont les domaines vitaux se chevauchent sont infectés et que les prévalences SIV dans les groupes peuvent dépasser 25%. Les virus touchant les gorilles du même groupe sont génétiquement proches montrant des liens épidémiologiques. Enfin, un suivi de l'infection réalisé de 2004 à 2009 sur un site a permis de découvrir un foyer d'infection, 2 cas de séroconversions et de retrouver une femelle gorille infectée à 5 ans d'intervalle. Dans ce site, la prévalence SIV est stable et le nombre de femelles infectées est plus important que le nombre de mâles. La structure sociale des gorilles et leur comportement peuvent alors expliquer en partie la répartition et la prévalence du SIVgor, ainsi que les différences avec l'infection chez les chimpanzés.Cette étude multidisciplinaire montre la faisabilité du suivi de l'infection SIV chez les gorilles en milieu naturel. Si le SIVgor est pathogène, le suivi pourra s'avérer essentiel chez cette espèce menacée d'extinction. / SIV infecting chimpanzees and gorillas are the precursors of the Human Immunodeficiency Virus type 1. The four groups of HIV-1 are the results of four different viral transmissions from apes to humans. Using non invasive methods we discovered the reservoir of HIV-1 M and N in two communities of chimpanzees (Ptt) in Cameroon and found that Gorillas (Ggg) are infected by a SIV close to HIV-1 O and P. While SIVgor has not yet been detected in chimpanzees, phylogeny shows that Ptt transmitted this virus to Ggg. Using a multidisciplinary approach, we studied the characteristics of the infection in wild living gorillas. We prospected 13 sites in Cameroon and 3 in CAR. 2120 fecal samples of gorillas and 442 of chimpanzees were collected. SIVgor infection was detected in 3 sites in Cameroon and the prevalence ranges from 3.2% to 4.6%, lower than in chimpanzees. Several social groups of gorillas with overlapping home-ranges were infected and the prevalence within group could exceed 25%. Viruses of the same group are genetically close, showing epidemiologic links. In a follow up study between 2004 and 2009 on one site, we discovered a focus of infection with 2 cases of seroconvertion and we re-sampled one infected female 5 years after. In this site, the prevalence of SIVgor is stable and the number of infected females is higher than the males. The social structure of gorillas and their behavior can partly explain for the repartition and prevalence of SIVgor, as well as the differences with the infection in chimpanzees. This multidisciplinary study proves the feasibility of a follow up study in wild living gorillas. If SIVgor turns out to be pathogenic, a follow up will be essential for this endangered species.

Les virus entérotropes sont des virus ubiquitaires infectant une large catégorie de vertébrés dont l’homme et les primates non-humains (PNHs). Ils se transmettent principalement par voie féco-orale directe ou indirecte à la suite de laquelle ils atteignent les entérocytes et s’y multiplient. Bien que parfois asymptomatiques, les infections causées par les virus entérotropes peuvent se manifester par des gastroentérites très fréquentes chez les enfants de moins de 5 ans. Ces mêmes virus peuvent être responsables de pathologies sévères telles que les maladies respiratoires, encéphalitiques, cardiaques, neurologiques. À partir des années 1950, de nombreux virus entérotropes ont été isolés de tissus de PNHs couramment utilisés en cultures cellulaires et en recherche biomédicale. Dès lors, de nombreuses études ont été conduites sur la caractérisation des virus entérotropes principalement chez les PNHs captifs ou en contact avec l’homme. En milieu naturel, en dehors des entérovirus et des adénovirus, leur circulation, leur épidémiologie et leur diversité restent encore peu connues. L’objectif de cette thèse est donc de rechercher et caractériser les virus entérotropes chez les PNHs d’Afrique Centrale. Ainsi à partir de 600 échantillons de fèces de PNHs collectés dans des forêts et réserves naturelles au Gabon, nous avons pu mettre en évidence la circulation de différentes espèces d’entérovirus (EVs) chez les mandrills et les chimpanzés. Cette caractérisation a également permis de mettre en évidence des EVs proches d’EVs infectant l’homme ainsi que deux nouveaux sérotypes chez un chimpanzé et chez un mandrill. Nous avons également mis en évidence un astrovirus (AstV) totalement divergent d’AstVs référencés chez un gorille. En dehors de leur circulation en milieu naturel, les virus entérotropes sont également présents chez les PNHs en contact fréquents avec l’homme. De ce fait à partir d’échantillons fécaux d’un groupe de 12 chimpanzés du Sanctuaire de Tchimpounga, nous avons caractérisé l’EV-C99 responsable de cas de paralysie chez l’homme et probablement responsable de celle observée chez un chimpanzé. De plus, deux sapovirus (SaVs) très proches d’un SaV identifié chez l’homme ont également été caractérisés. L’Afrique Centrale est donc caractérisée par une diversité de virus entérotropes qui circulent chez les PNHs. L’identification chez les PNHs de virus entérotropes proches en milieu naturel de ceux infectant l’homme soulève l’existence d’une probabilité de transmission inter-espèce entre les PNHs et l’homme dont le sens reste encore à déterminer. Par contre chez les PNHs du sanctuaire, la susceptibilité à ces virus humains peut être responsable de pathologies graves comme la paralysie observée chez les chimpanzés. / The enteric viruses are ubiquitous virus infecting a broad range of vertebrates, including humans and non-human primates (NHPs). They are spread by direct or indirect fecal-oral route following which they reach the enterocytes and multiply. Even though infections caused by these viruses are asymptomatic, enteric viruses could be responsible for frequent gastroenteritis in children under 5 years of age. These viruses may be responsible for severe pathologies such as respiratory, encephalitic, cardiac and neurological diseases. In the 1950s, many viruses have been isolated from NHPs species commonly used in cell culture and biomedical research. Since, many studies have been conducted to characterize, then enteric viruses have been mainly identified in captive NHPs or those living in close contact with humans. Little is known concerning the circulation, epidemiology and diversity of enteric viruses in the wild, except for enteroviruses and adenoviruses. The objective of this thesis is to investigate and characterize the enteric virus in NHPs of Central Africa. Thus from 600 samples of feces of NHPs collected in natural forests and reserves in Gabon, we highlighted the circulation of different species enteroviruses (EVs) in mandrills and chimps. We also identified EVs close to those infecting humans as well as two new serotypes in a chimpanzee and in a mandrill. We have highlighted an astrovirus (AstV) completely divergent from those referenced in a gorilla. Apart from their outstanding natural environment, enteric viruses are also present in NHPs in frequent contact with humans. Therefore fecal samples from a group of 12 chimpanzees from the Tchimpounga Sanctuary, we characterized the EV-C99 responsible for cases of paralysis in humans and probably responsible for that observed in a chimpanzee. In addition, two sapovirus (SaVs) very close to a SaV identified in humans have also been characterized. Central Africa is therefore characterized by a diversity of enteric virus circulating in NHPs. The identification in the wild of enteric virus in NHPs close to those infecting humans raises probability of cross-species transmissions between NHPs and humans whose sense remains to be determined. However in NHPs in the sanctuary, susceptibility to these human viruses can be responsible for severe diseases such as paralysis observed in chimpanzee.

Philosophiae Doctor - PhD / The use of ontologies in the mapping of gene expression events provides an effective and comparable method to determine the expression profile of an entire genome across a large collection of experiments derived from different expression sources. In this dissertation I describe the development of the developmental human and mouse eVOC ontologies and demonstrate the ontologies by identifying genes showing a bias for developmental brain expression in human and mouse, identifying transcription factor complexes, and exploring the mouse orthologs of human cancer/testis genes.Model organisms represent an important resource for understanding the fundamental aspects of mammalian biology. Mapping of biological phenomena between model organisms is complex and if it is to be meaningful, a simplified representation can be a powerful means for comparison. The implementation of the ontologies has been illustrated here in two ways.Firstly, the ontologies have been used to illustrate methods to determine clusters of genes showing tissue-restricted expression in humans. The identification of tissue restricted genes within an organism serves as an indication of the finetuning in the regulation of gene expression in a given tissue. Secondly, due to the differences in human and mouse gene expression on a temporal and spatial level, the ontologies were used to identify mouse orthologs of human cancer/testis genes showing cancer/testis characteristics. With the use of model systems such as mouse in the development of gene-targeted drugs in the treatment of disease, it is important to establish that the expression characteristics and profiles of a drug target in the model system is representative of the characteristics of the target in the system for which it is intended.

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As novel or variant strains of HEV continue to evolve rapidly both in humans and other animals, it is important to develop a rapid pre-sequencing screening method to select field isolates for further molecular characterization. Two heteroduplex mobility assays (HMA) were developed to genetically differentiate field strains of swine HEV and avian HEV from known reference strains. It was shown that the HMA profiles generally correlate well with nucleotide sequence identities and with phylogenetic clustering between field strains and the reference swine HEV or avian HEV strains. Therefore, by using different HEV isolates as references, the HMA developed in this study can be used as a pre-sequencing screening tool to identify variant HEV isolates for further molecular epidemiological studies. Our previous study showed that avian HEV antibody is prevalent in apparently healthy chickens. A prospective study was conducted on a known seropositive but healthy chicken farm. Avian HEV was identified from the healthy chicken flock. Avian HEV isolates recovered from the healthy chicken share 70-97% nucleotide sequence identities with those isolates which cause hepatitis-splenomegaly (HS) syndrome based on partial helicase and capsid gene regions. Recovery of identical viruses from the experimentally inoculated chickens in the subsequent transmission study further confirmed our field results. The capsid gene of avian HEV isolates from chickens with HS syndrome were also characterized and found to be heterogeneic, with 76-100% nucleotide sequence identities to each other. The study indicates that avian HEV is enzootic in chicken flocks and spread subclinically among chicken populations, and that the virus is heterogeneic. As HEV can not be propagated <i>in vitro</i>, in order to further characterize avian HEV, an infectious viral stock with a known infectious titer must be generated. Bile and feces collected from specific-pathogen-free (SPF) chickens experimentally infected with avian HEV were used to prepare an avian HEV infectious stock. The infectivity titer of this infectious stock was determined, by intravenously inoculating one-week old SPF chickens, to be 5 x 10^4.5 50% chicken infectious doses (CID₅₀) per ml. Seroconversion, viremia as well as fecal virus shedding were observed in the inoculated chickens. Contact control chickens also became infected via direct contact with inoculated ones. Avian HEV infection in chickens was found to be dose-dependent. To determine if avian HEV can infect across species, one-week old SPF turkeys were intravenously inoculated each with 10^4.5(CID₅₀) of avian HEV. The inoculated turkeys seroconverted to avian HEV antibodies at 4-8 weeks postinoculation (WPI). Viremia was detected at 2-6 WPI, and fecal virus shedding at 4-7 WPI in inoculated turkeys. This is the first demonstration of cross-species infection by avian HEV. Little is known regarding the characteristics of the small ORF3 protein largely due to the lack of a cell culture system for HEV. To characterize the small protein, the ORF3 proteins of avian HEV and swine HEV were expressed in <i>Escherchia coli</i>, and purified by BugBuster His-Bind Purification System. Western blot analysis showed that avian HEV ORF3 protein is unique and does not share common antigenic epitopes with those of swine HEV and human HEV. However, swine HEV (genotype 3) and human HEV (genotype 1) ORF3 proteins cross-react with each other antigenically. To determine if the ORF3 protein is a virion protein, infectious stocks of avian HEV and swine HEV were first generated in SPF chickens and pigs, respectively. Virions were subsequently purified by sucrose density gradient centrifugation and virion proteins were characterized by SDS-PAGE and Western blot analysis. Two major forms of ORF2 proteins of avian HEV were identified: a 56 kDa and an 80 kDa proteins. Multiple immunoreactive forms of ORF2 proteins of swine HEV were also observed: 40 kDa, 53 kDa, 56 kDa and 72 kDa. However, the ORF3 protein was not detected from the native virions of avian HEV or swine HEV. These findings provide direct evidence that ORF2 indeed encodes a structural protein of HEV, whereas ORF3 does not. To search for other potential animal reservoirs for HEV, the prevalence of IgG anti-HEV antibody was determined in field mice caught in chicken farms to assess the possibility of mice as a potential reservoir for HEV infection in chickens. Three different recombinant HEV antigens derived from avian HEV, swine HEV, and human HEV were used in the ELISA assays. The anti-HEV seropositive rates in wild field mice (<i>Mus musculus</i>), depending upon the antigen used, are 15/76 (20%), 39/74 (53%), and 43/74 (58%), respectively. HEV RNA was also detected from 29 fecal and/or serum samples of mice. The HEV sequences recovered from field mice shared 72-100% nucleotide sequence identities with each other, 73-99% sequence identities with avian HEV isolates, and 51-60% sequence identities with representative strains of swine and human HEVs. However, attempts to experimentally infect laboratory mice (Mus musculus) with the PCR-positive fecal materials recovered from the wild field mice were unsuccessful. We also attempted to experimentally infect 10 Wistar rats each with avian HEV, swine HEV, and an US-2 strain of human HEV, respectively. However, the inoculated rats did not become infected as evidenced by the lack of viremia, virus shedding in feces or seroconversion. These data suggest that mice caught in chicken farms are infected by a HEV-like virus, but additional work is needed to determine the origin of the mouse virus as well as the potential role of rodents in HEV transmission. In summary, we developed two HMAs which are useful for differentiation and identification of variant strains of swine and avian HEVs. We genetically identified and characterized an avian HEV strain from apparently healthy chickens in seropositive flocks. We showed that avian HEV can cross species barriers and infect turkeys. Our data indicated that avian and swine HEV ORF2 genes encode structural proteins, whereas ORF3 genes do not. Evidence in this study also showed that HEV or HEV-like agent exists in field mice on a chicken farm. / Ph. D.

Hepatitis E Virus (HEV), the causative agent of hepatitis E, is a zoonotic pathogen of worldwide significance. The genus Orthohepevirus A of the family Hepeviridae includes all mammalian strains of HEV and consists of 8 recognized genotypes. Genotypes 1 and 2 HEVs only infect humans and genotypes 3 and 4 infect humans and several other animal species including pigs and rabbits. An ever-expanding host range of genetically-diversified strains of HEV now include bat, fish, rat, ferret, moose, wild boar, mongoose, deer, and camel. Additionally, the ruminant species goats, sheep, and cattle have been implicated as potential reservoirs as well. My dissertation research investigates a novel animal model for HEV, examines the immune dynamics during acute infection, and evaluates the possibility of additional animal reservoirs of HEV. The first project established an immunoglobulin (Ig) heavy chain knock-out JH (-/-) gnotobiotic piglet model that mimics the course of acute HEV infection observed in humans and evaluated the pathogenesis of HEV infection in this novel animal model. The dynamics of acute HEV infection in gnotobiotic pigs were systematically determined with a genotype 3 human strain of HEV. We also investigated the potential role of immunoglobulin heavy-chain JH in HEV pathogenesis and immune dynamics during the acute stage of virus infection. This novel gnotobiotic pig model will aid in future studies into HEV pathogenicity, an aspect which has thus far been difficult to reproduce in the available animal model systems. The objective of the second project for my PhD dissertation was to determine if cattle in the United States are infected with a bovine strain of HEV. We demonstrated serological evidence of an HEV-related agent in cattle populations with a high level of IgG anti-HEV prevalence. We demonstrated that calves from a seropositive cattle herd seroconverted to IgG binding HEV during a prospective study. We also showed that the IgG anti-HEV present in cattle has an ability to neutralize genotype 3 human HEV in vitro. However, our exhaustive attempts to detect HEVrelated sequence from cattle in the United States failed, suggesting that one should be cautious in interpreting the IgG anti-HEV serological results in bovine and other species. Collectively, the work from my PhD dissertation delineated important mechanisms in HEV pathogenesis and established a novel animal model for future HEV research. / Ph. D. / Hepatitis E Virus (HEV), the causative agent of hepatitis E, is a zoonotic pathogen of worldwide significance. According to the World Health Organization, there are approximately 20 million HEV infections annually, which result in 3.3 million cases of acute hepatitis E and >44,000 HEV-related deaths. Hepatitis E is a self-limiting acute disease in general, but carries the ability to cause high mortality in pregnant women and chronic hepatitis in immunocompromised individuals. The underlying mechanisms of HEV host tropism and progression of disease to chronicity are unknown. My dissertation work investigates a novel animal model for HEV, evaluates the possibility of additional animal reservoirs of HEV, and examines the immune dynamics during acute infection. The first project established an immunoglobulin (Ig) heavy chain knock-out JH (-/-) gnotobiotic piglet model that mimics the course of acute HEV infection observed in humans. The dynamics of acute HEV infection were determined in both the knock-out and wild-type piglets with a genotype 3 strain of human HEV. We also investigated the potential role of immunoglobulin heavy-chain JH in HEV pathogenesis and virus infection. In the second project, we determined if cattle in the United States are infected with a bovine strain of HEV. We showed serological evidence of an HEV-related agent in cattle as well as calves born in a seropositive herd. Despite the detection of specific antibodies recognizing HEV in cattle, definitive evidence of virus infection could not be demonstrated. Our exhaustive attempts to detect HEV-related sequence from cattle in the United States failed, suggesting that one should be cautious in interpreting the IgG anti-HEV serological results in bovine and other species. Collectively, the work from my PhD dissertation research delineated important mechanisms in HEV pathogenesis and established a novel animal model for future HEV research.

Depuis la découverte du virus de l'Immunodéficience humaine, un lentivirus, comme agent pathogène responsable de l'épidémie du SIDA en 1983, beaucoup de progrès sur le sujet ont été réalisés. Il existe deux types de virus différents pouvant infecter l'Homme, le HIV-1 et le HIV-2. Ces deux virus se regroupent en différents groupes et sous-types qui témoignent d'une grande diversité inter et intra individus (notions de quasi-espèces). La découverte de lentivirus infectant naturellement au moins quarante-cinq espèces de primates en Afrique sub-saharienne, a permis un enrichissement des connaissances sur les origines des épidémies lentivirales humaines. Aujourd'hui , il est clairement admis que l'origine des épidémies d'HIV-1 et HIV-2 sont le résultat de transmissions zoonotiques de virus de chimpanzés/gorilles et de mangabeys enfumées, respectivement. La mise en évidence de nombreux SIV circulant chez ces primates non-humains indique bien le risque potentiel de nouvelles zoonoses dans la population humaine exposée, cependant, il peut paraître surprenant que jusqu'à maintenant, deux lignées lentivirales seulement ont été capables de franchir cette barrière d'espèce. Pour pouvoir se répliquer dans les cellules d'un nouvel hôte, un lentivirus doit pouvoir contrecarrer les différents facteurs de restriction exprimés par les cellules cibles tout en exploitant au maximum la machinerie cellulaire. La famille de protéines TRIM5, APOBEC3 et les protéines Tetherin/Bst2 et SAMHD1 sont capables de bloquer une infection rétrovirale. Dans ce travail, le rôle des protéines TRIM5 a été étudié ainsi que celui d'autres protéines interagissant avec des capsides rétrovirales, dans un contexte de transmission inter-espèces de lentivirus de primates. L'étude de TRIM5α humain a montré que cette protéine n'était capable de bloquer aucune des infections par les lentivirus primates testés dans cette étude, ni par les autres SIV. Nous avons pu mettre en évidence que la dépendance de la liaison à la Cyclophiline A pour l'infection des différents SIV était variable en fonction de la capside testée. Ainsi, si cette interaction est largement répandue parmi les différentes lignées de SIV, elle n'est toutefois pas universelle. La sensibilité des SIV à la déplétion de nucléoporines qui sont connues pour affecter l'infection par HIV-1, était également variable pour différents SIV, et la même diversité a été observée concernant les déplétions de RanBP2 et Nup153. De plus, nous avons découvert une capside de SIV soumise à une forte restriction de son infection dans les cellules humaines, ce phénotype a été nommé Ref2.Il a été suggéré qu'il existait une possible corrélation entre des variations de la capside de HIV-2 et la progression vers le SIDA, nous avons donc élaboré une étude afin de déterminer si les protéines TRIM5 étaient impliquées dans ce phénotype. La conclusion est que TRIM5α humaine ne restreint fortement aucune des capsides de HIV-2 testées provenant d'une cohorte d'individus à “progression rapide“ ou “lente“ vers le SIDA. Cependant nous avons observé une capacité d'infection qui corrélait avec la pathogénicité. Il est intéressant de noter que toutes les capsides d'HIV-2 testées étaient dépendantes de la présence de Cyclophiline A pour leur infection. Toutes ces capsides étaient sensibles à la déplétion de RanBP2, et l'interaction est très probablement médiée par le motif C-ter de RanBP2 qui a une forte homologie avec la Cyclophiline A. En conclusion, il est très probable que des SIV infectant naturellement des singes puissent utiliser les mêmes protéines que HIV-1, pour un éventuel passage inter-espèces. TRIM5α ne semble pas être une barrière efficace aux différents SIV, et l'interaction avec la Cyclophiline A est probablement très conservée par les lentivirus primates / Ever since HIV has been discovered to be the pathogenic agent that causes AIDS in 1983, much progress has been made in the field. Two different viruses are now known to infect humans, HIV-1 and HIV-2. These two distinct viruses have many sub-types and clades representing a high diversity inter and intra-individuals (quasi-species). The finding of HIV simian counterparts, the Simian Immunodeficiency Viruses (SIVs), has broadened the knowledge of primate lentiviruses and to date forty-five species of non-human primates are known to be infected with SIVs in sub-saharan Africa. It is now clear that HIV-1 and HIV-2 epidemics are the result of zoonosis from chimpanzees/gorillas and sooty mangabeys, respectively. With such a big diversity of SIVs in the wild and a frequent contact of SIV infected monkey species with humans, it is interesting that so far, only two lineages breached the species barrier and infected human populations. To be able to correctly infect a cell, a lentivirus has to overcome the installed cellular barriers known as restriction factors while at the same time correctly exploiting the established host cellular machinery. Proteins such as TRIM5, APOBEC3, Tetherin/Bst2, SAMHD1 are able to restrict retroviral infections in certain conditions. In this thesis, it has been evaluated the role of TRIM5 proteins and other capsid interacting proteins with a scope to the eventuality of a cross-species transmission infection. The results showed that human TRIM5alpha does not restrict any of the primate lentiviruses tested, and so far, no primate lentivirus is known to be restricted by it. Cyclophilin A binding and dependence is variable depending on the SIV capsid; this interaction is widespread among the primate lentiviruses phylogenetic tree but not a universal phenotype. Different capsids from SIVs have been tested for the sensitivity to the depletion of nucleoporins that are known to be used by HIV-1 in its infection; it has been concluded that the same diversity applies to the interaction with RanBP2 and Nup153. Additionally, we identified a SIV capsid that is highly restricted in human cells; this phenotype was called Ref2. With the report of a possible correlation between HIV-2 capsid variations and different levels of progression to AIDS, we devised a study aiming to identify if TRIM5 proteins were involved in this phenotype. We concluded that human TRIM5alpha does not restrict any HIV-2 capsid obtained from a HIV-2 cohort, in which individuals were presenting different levels of progression to AIDS. However, we observed a different viral fitness that correlated with pathogenicity. Moreover, Cyclophilin A dependence seems ubiquitous among all of the tested HIV-2 capsids. All of these capsids are sensitive to RanBP2 depletion and the interaction is much likely mediated by RanBP2's C-terminal motif that shares a high homology with Cyclophilin A. Summing up, it is much likely that some SIVs that still circulate in the wild can hijack the same specific cellular co-factors as HIV-1 to produce a new epidemic in humans. TRIM5α does not seem to be a potent barrier to an eventual cross-species transmission from lower primates to humans, and Cyclophilin A interaction seems to play a major role to the infection of some SIVs.