Teses / dissertações sobre o tema "Lentivirusus"
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Robertson, David L. "Recombination in primate lentiviruses". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336866.
Texto completo da fonteVödrös, Dalma. "Receptor use of primate lentiviruses /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-497-6/.
Texto completo da fonteBailes, Elizabeth. "Origins and evolution of primate lentiviruses". Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246384.
Texto completo da fonteCordeil, Stéphanie. "Etude de la différence de susceptibilité des lentivirus de primates aux interférons de type I". Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0781.
Texto completo da fonteType I Interferons (IFN-α/β, herein IFNs) provide an important mechanism of defense against pathogens and regulate in a paracrine and autocrine manner both intrinsic and adaptive immune responses. In the case of HIV-1 however, the relationship between IFNs and viral replication appears more complex. Indeed, if IFNs have been described to interfere with HIV-1 at basically all phases of its life cycle ex vivo, an IFN-induced state is linked to AIDS progression and to high viral loads in HIV-1 infected individuals. Similarly, a deregulated and prolonged IFN production/state seems one of the main distinguishing features between pathogenic and non-pathogenic SIV infection in primate animal models, suggesting that a deregulated IFN-state may be more detrimental to the host than to the virus itself in vivo.If this hypothesis is correct and if HIV-1 plays an active role in the perpetration of this antiviral state, it is possible that HIV-1 may have overall evolved to cope with this environment, remaining able to replicate despite it.To determine whether HIV-1 was better armed to replicate in the presence of an IFN-state environment than other primate lentiviruses, we compared HIV-1 to SIVmac and more importantly to HIV-2 that albeit capable of inducing AIDS in humans does so in a much less aggressive manner. In agreement with the initial hypothesis, our results indicate that HIV-1 is better fit to replicate in primary cells in the presence of amounts of IFN comparable to the ones measured in vivo, while the replication of HIV-2/SIVmac viruses is completely blocked even in the presence of low levels of IFN. By decorticating the effects of IFNs on the early and late phases of the viral life cycle in primary macrophages, we show here that the main target of the differential action of IFNs are the early phases of infection. More specifically, with time kinetics that we determine herein, IFNs induce cellular factor/s that differentially affect the stability of pre-reverse transcription complexes of HIV-2, but not of HIV-1. Our results could underlie a different evolutionary adaptation of primate lentiviruses to interferons that might be responsible for their different pathogenicity in vivo
Gelinas, Jean-Francois. "Enhancement of lentiviral vector production through alteration of virus-cell interactions". Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:9921b8b4-e2b5-4eec-9efc-6036765c8d55.
Texto completo da fonteKelly, Maureen C. "Parallels in tRNA primer acquisition by lentiviruses". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/kelly.pdf.
Texto completo da fonteMartin, Michaël. "Mécanisme moléculaire de l'antagonisme du complexe HUSH par les protéines lentivirales Vpx et Vpr". Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5160.
Texto completo da fonteHIV-1 and HIV-2, lentiviruses responsible for AIDS, appeared in humans after cross-species transmissions from simian viruses (SIV). In addition to their structural and regulatory proteins, lentiviruses encode auxiliary proteins that promote viral replication in the host cell by counteracting antiviral cellular factors, called restriction factors. The mechanism of action of these viral auxiliary proteins often relies on the hijacking of Ubiquitin-Ligase complexes, a mechanism widely used by various pathogens, to degrade host cell proteins. This mechanism is used by the Vpx protein, expressed only by HIV-2 (and not by HIV-1), which induces the degradation of SAMDH1, a restriction factor blocking the reverse transcription step. Thus, Vpx molecularly bridges the DCAF1 adaptor of the Cul4A-DDB1(DCAF1) Ubiquitin-Ligase complex with SAMHD1, resulting in ubiquitination and degradation of SAMHD1. In 2018, our team showed that Vpx induces the degradation of an additional cellular factor: the HUSH complex, composed of TASOR, MPP8 and Periphilin. This complex is involved in the epigenetic repression not only of many cellular genes, retro-transposable elements and endogenous retroviruses, but also of the HIV genome integrated into the infected cell. By degrading HUSH, Vpx promotes viral expression. In this context, the objectives of my thesis were to: (i) Determine whether HUSH degradation mechanism induced by HIV-2 Vpx was identical to SAMHD1 degradation mechanism. I was able to highlight important differences between the two mechanisms although Vpx uses, in both cases, the same Ubiquitin-Ligase adaptor, DCAF1 (main focus of the thesis work, submitted article). (ii) Characterize the molecular determinants involved in the antagonism of HUSH by other lentiviral proteins. First, we wanted to know if different Vpx-related viral proteins, in various simian virus species, had the same capacity to degrade the HUSH complex. This allowed us to reveal a lentiviral species-specificity of HUSH complex antagonism, a major characteristic of restriction factors (contribution to Chougui et al., Nature microbiology, 2018). Secondly, this led me to start studying the viral determinants of these Vpx-related proteins, such as the Vpr proteins from different strains of SIVagm (infecting the African green monkey) that present different phenotypes regarding both SAMHD1 or HUSH degradation (work in progress). All the results allowed us to better characterize the mechanism of HUSH antagonism by Vpx/Vpr lentiviral proteins, and to provide the first molecular tools to differentiate HUSH antagonism from SAMHD1 antagonism in primary cells. In the future, these data may help to better understand how various lentiviral proteins have adapted to their different cellular substrates (and vice versa) along evolution. Finally, targeting HUSH through the identification of interaction or degradation determinants could be interesting for the development of new therapeutic targets
Li, Li. "Short-term and long-term evolution of lentiviruses". Thesis, University of Nottingham, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.575475.
Texto completo da fonteLee, Wei-Cheng. "Studies on lentivirus infection of macrophages". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/29845.
Texto completo da fonteStarling, Isabella. "Mechanisms and specificity of lentivirus neurotoxicity". Thesis, University of Edinburgh, 1998. http://webex.lib.ed.ac.uk/abstracts/starli01.pdf.
Texto completo da fonteBurkala, Evan Jon. "Investigations of the Australian bovine lentivirus". Thesis, Burkala, Evan Jon (2001) Investigations of the Australian bovine lentivirus. PhD thesis, Murdoch University, 2001. https://researchrepository.murdoch.edu.au/id/eprint/41607/.
Texto completo da fonteHarris, Matthew E. "Analysis of post-transcriptional regulation of lentiviruses and mammalian hepadnaviruses /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9935471.
Texto completo da fonteBroughton-Neiswanger, Liam E. "Maternal transmission is the major mode of ovine lentivirus transmission in a ewe flock a molecular epidemiology study /". Pullman, Wash. : Washington State University, 2010. http://www.dissertations.wsu.edu/Thesis/Spring2010/L_Broughton_042010.pdf.
Texto completo da fonteTitle from PDF title page (viewed on June 29, 2010). "College of Veterinary Medicine." Includes bibliographical references (p. 20-26).
Stewart, Meredith Ellen. "An investigation into aspects of the replication of Jembrana disease virus /". Access via Murdoch University Digital Theses Project, 2005. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20051222.104106.
Texto completo da fonteBichel, Katsiaryna. "Understanding post-entry pre-integration lentiviral biology". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648287.
Texto completo da fonteCamacho, Emely. "Optimization of Lentivirus Production for Cancer Therapy". Thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-164715.
Texto completo da fonteParker, Douglas George Anthony, e park0290@flinders edu au. "Lentivirus-mediated gene expression in corneal endothelium". Flinders University. Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20081204.094431.
Texto completo da fonteMAZARIN, VERONIQUE. "Etude d'un gene precoce du lentivirus visna". Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX22964.
Texto completo da fonteFeyertag, Felix. "Evolutionary dynamics of lentiviruses associated with drug resistance and host adaptation". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/evolutionary-dynamics-of-lentiviruses-associated-with-drug-resistance-and-host-adaptation(cf1aaffa-c1c2-450d-8d25-538c0bcc0d02).html.
Texto completo da fontePernot, Eileen. "Etude in vivo du rôle de la 5-phosphatase de phosphoinositides SKIP". Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210473.
Texto completo da fonteDes études de surexpression de SKIP en cellules tendent à montrer que cette protéine pourrait jouer un rôle de régulateur négatif dans la formation du cytosquelette d’actine et/ou dans la voie de signalisation de l’insuline.
Afin d’étudier in vivo la fonction de la protéine SKIP chez la souris, nous avons décidé de générer des souris transgéniques surexprimant cette protéine de manière conditionnelle. Dans ce but, nous avons infecté des embryons murins par des lentivirus porteurs d’un transgène SKIP et avons obtenu, après réimplantation des embryons infectés dans des femelles pseudogestantes, deux lignées de souris transgéniques. Celles-ci ont ensuite été croisées avec des souris exprimant la recombinase Cre de manière ubiquitaire afin de pouvoir activer la transcription de SKIP dans l’ensemble des organes. Des expériences de Western blot, de dosage d’activité 5-phosphatase ainsi que des PCR en temps réel sont venus confirmer la présence de la protéine transgénique et de son activité catalytique.
L’ensemble des expériences qui ont été menées du point de vue phénotypique tend à montrer que dans notre modèle, la surexpression de SKIP ne provoque aucune anomalie évidente du point de vue anatomique, glycémique ou immunologique. Toutefois, des expériences concernant la physiologie rénale ont été réalisées sur base des résultats d’immunohistochimie et nous ont permis de détecter une anomalie dans les mécanismes de réabsorption d’eau ainsi que dans l’expression et la phosphorylation des canaux hydriques AQP2.
Doctorat en Sciences
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Ditcham, William. "The development of recombinant vaccines against Jembrana disease". Thesis, Ditcham, William (2007) The development of recombinant vaccines against Jembrana disease. PhD thesis, Murdoch University, 2007. https://researchrepository.murdoch.edu.au/id/eprint/438/.
Texto completo da fonteDitcham, William. "The development of recombinant vaccines against Jembrana disease". Ditcham, William (2007) The development of recombinant vaccines against Jembrana disease. PhD thesis, Murdoch University, 2007. http://researchrepository.murdoch.edu.au/438/.
Texto completo da fonteCarnell, George William. "Development of hybrid haemagglutinin pseudotyped lentiviruses to assess heterosubtypic immunity to influenza". Thesis, University of Kent, 2017. https://kar.kent.ac.uk/66363/.
Texto completo da fonteStivahtis, Gina Lynn. "The role of Vpr in cell-cycle regulation by diverse primate lentiviruses /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/5017.
Texto completo da fonteZhu, Xiaonan. "Identification of the Function of the Vpx Protein of Primate Lentiviruses: A Dissertation". eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/447.
Texto completo da fonteVink, C. A. "A hybrid lentivirus-transposon vector for safer gene therapy". Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19233/.
Texto completo da fonteLerondelle, Catherine. "Les infections mammaires à lentivirus chez les petits ruminants". Lyon 1, 1992. http://www.theses.fr/1992LYO10210.
Texto completo da fonteBodungen, Uta von. "Immunohistology of the early course of lentivirus-induced arthritis /". [S.l.] : [s.n.], 1996. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Texto completo da fonteau, w. ditcham@murdoch edu, e William Ditcham. "The development of recombinant vaccines against Jembrana disease". Murdoch University, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20071119.94111.
Texto completo da fonteSetiyaningsih, Surachmi. "Molecular and immunogenic analysis of Jembrana disease virus Tat". Thesis, Setiyaningsih, Surachmi (2006) Molecular and immunogenic analysis of Jembrana disease virus Tat. PhD thesis, Murdoch University, 2006. https://researchrepository.murdoch.edu.au/id/eprint/299/.
Texto completo da fonteSetiyaningsih, Surachmi. "Molecular and immunogenic analysis of Jembrana disease virus Tat". Setiyaningsih, Surachmi (2006) Molecular and immunogenic analysis of Jembrana disease virus Tat. PhD thesis, Murdoch University, 2006. http://researchrepository.murdoch.edu.au/299/.
Texto completo da fonteVabret, Nicolas. "Hypothèses sur l'implication du biais nucléotidique des lentivirus dans le développement du SIDA et nouvelles stratégies d'atténuation du VIH-1". Thesis, Lyon, École normale supérieure, 2011. http://www.theses.fr/2011ENSL0649.
Texto completo da fonteAfter over thirty years of AIDS epidemic, we still need to identify immunological correlates of protection against AIDS and we do not properly understand how HIV causes AIDS in infected individuals. In order to reproduce the protective capacity of live attenuated viruses, we first aimed at generating a hybrid virus structurally similar to HIV-1 and able to replicate exclusively in the cytoplasm of infected cells. We developed new polioviral pluricistronic vectors that contain HIV-1 packaging sequences, gag gene and/or env gene. We then showed that the use of these replicons was compatible with the production of processed and mature HIV structural proteins. Secondly, we investigated the consequences of the lentivirus nucleotide composition (% A/T/G/C) bias on their pathogenicity. We found a correlation, indicating that AIDS results from infection by primate lentiviruses having the most divergent nucleotide composition compared to their hosts, whereas less divergent lentiviruses cause non-pathogenic infections. A strong type I interferon (IFN-I) response during the chronic phase of infection is a typical feature of lentiviral pathogenic infection. We showed that nucleotide optimization of lentiviral RNA sequences dramatically reduce their in vitro capacity to induce IFN-I. We synthesized a simian immunodeficiency virus (SIV), whose genome sequence was artificially optimized to the macaque average nucleotide composition. This virus showed a reduced capacity to stimulate IFN-I in vitro than wt SIV. These data indicate for the first time a link between the nucleotide composition of lentiviruses and their pathogenicity. They suggest new vaccine attenuation strategies against AIDS
He, Jin. "Lentiviral vectors mechanisms of transgene silencing and functional characterization of novel genes /". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006628.
Texto completo da fonteTypescript. Title from title page of source document. Document formatted into pages; contains 143 pages. Includes Vita. Includes bibliographical references.
Chettab, Abdelkamel. "Utilisation de constructions plasmidiques pour l'investigation des interactions entre les lentivirus des petits ruminants et leurs hôtes in vivo et in vitro". Lyon 1, 1997. http://www.theses.fr/1997LYO1T107.
Texto completo da fonteTristem, Michael. "Sequence of a novel isolate of HIV-2 and its relationship to other lentiviruses". Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239787.
Texto completo da fontePryszlak, Anna Marta [Verfasser], e Felix [Akademischer Betreuer] Hoppe‐Seyler. "Functional Crosstalk between Human Papillomaviruses and Lentiviruses / Anna Marta Pryszlak ; Betreuer: Felix Hoppe‐Seyler". Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180607856/34.
Texto completo da fonteRolland, Morgane. "Etude des relations phylogénétiques entre les lentivirus des petits ruminants". Bordeaux 2, 2003. http://www.theses.fr/2003BOR21029.
Texto completo da fonteTo facilitate the study of SRLV, we established a GSM T ("goat synovial membrane") cell line by the ectopic expression of telomerase. Cultures of GSM T cells have been passaged over 160 times without showing any phenotypic difference from the original primary GSM cells. Moreover, the immortalized GSM T cells were susceptible to infection by both CAEV and MVV and were able to propagate these viruses. We also optimized a PCR protocol to amplify the SRLV genome as a whole or with two overlapping fragments. To address the genetic diversity and relatedness among SRLV strains worldwide, we applied extensive phylogenetic methods to the sequences available together with our newly characterized sequences from Ireland and Spain. The Irish lentivirus strain, which was isolated from a goat, was more closely related to the lentivirus that infects sheep : MVV. The four Spanish ovine isolates fell in three distinct clusters, which clearly depicted the major genetic variability seen in Spain. Based on the phylogenetic analyses in the gag, pol and env regions, we revise the classification of the SRLV, which could be confidently classified into five clades rather than six as it was previously suggested. Furthermore, we observed that MVV and CAEV sequences could not be phylogenetically distinguished according to their host. Therefore, we propose to group the two viruses more appropriately as SRLV
Gourdou, Isabelle. "Le lentivirus Visna : étude de ses gènes de régulation précoces". Aix-Marseille 1, 1990. http://www.theses.fr/1990AIX11291.
Texto completo da fontePuissant, Bénédicte. "Etude de facteurs génétiques susceptibles d'influencer l'infection par les lentivirus". Toulouse 3, 2005. http://www.theses.fr/2005TOU30036.
Texto completo da fonteHost genetic factors greatly influence the disease progression in human and primates infected with HIV (Human Immunodeficiency Virus) or SIV (Simian Immunodeficiency Virus). We studied the polymorphism of chemokine genes and chemokine receptor genes in human and we showed that these polymorphisms did not influence the virological response to antiretroviral treatment. We also showed that these genes are polymorphic in the eight primate species we studied. We analyzed the polymorphism of blood group glycosyltransferases in HIV-infected patients and we observed that the frequency of Lewis positive individuals was lower among HIV-infected patients than among healthy controls. This could suggest a protective effect of Lewis antigens against HIV infection. Finally, we analyzed the gene expression of human and chimpanzee CD4 T cells infected in vitro by HIV and we identified genes that could explain the resistance of chimpanzee to HIV induced disease
Barban, Véronique. "Etude du contenu génétique et de l'expression des lentivirus animaux". Grenoble 2 : ANRT, 1986. http://catalogue.bnf.fr/ark:/12148/cb37595704k.
Texto completo da fonteAhmid, Simaa. "Analyse fonctionnelle de génomes lentiviraux de primates réplicatifs sous le contrôle des promoteurs du lentivirus caprin CAEV : Modèle d'étude pour la latence et persistance des lentivirus". Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV018/document.
Texto completo da fonteAcquired Immuno-Deficiency Syndrome (AIDS) is a disease caused by immunodeficiency viruses in human (HIV-1) and some animal species. The virus is a small enveloped particle that has a single-strand RNA genome and belongs to the lentivirus genus that belongs to the Retroviridae family. In human the virus infects and replicates mainly in cells that express the CD4 on their surface. Since its apparition in human in 1982 the virus has infected around 80 million individuals worldwide and caused the death of nearly half of them. No vaccine exists but life expectancy of near half of HIV-1-infected individuals has been now prolonged due to extensive highly active antiretroviral therapy (HAART). Because of the complexity of the host/pathogen interactions that are associated with HIV-1 infection in human and non-human primate models, a simple model system is strongly needed to ease the studies aiming at better understanding the underlying mechanisms of increased pathogenesis of HIV-1 in human. A chimeric virus CAL-HIV-R1 was created in our laboratory by exchanging the long terminal repeats (LTRs) of HIV with those of CAEV, a caprine lentivirus. Because these CAEV LTRs have a constitutive promoter, which is independent of the trans-activator of transcription, we expect that this chimeric virus should not undergo latency in memory CD4+ T cells. To increase the potency of this chimera, serial passages on cultured human cells were performed. Besides its primary receptor, CD4, HIV needs to interact with another molecule as a co-receptor. Several infectious molecular clones of HIV-1 isolates pDNAs containing the complete proviral genomes were received from the NIH AIDS Reagent Program Repository. Three of these, namely pNL4-3, p89.6 and WARO, were used to produce virus stocks following transfection in the human HEK-293T cell line and used to infect a variety of cell lines such as: 1) GHOST cells that were used to examine the tropism for the co-receptor that were X4, X4/R5 and R5 respectively; 2) M8166 a fusogenic indicator cell line to evaluate the replication competency, 3) TZM-bl to determine the infectivity titers of the viruses by scoring the blue cells enabled by infections. A vaccine based on a chimeric DNA vector, CAL-SHIV-IN-, has been developed in our laboratory and tested in macaques. A sero-neutralization assay was performed on sera of macaques, which had been vaccinated with this vector and challenged in parallel with control animals with a pathogenic virus. This assay was used to verify the presence of neutralizing antibodies, but, unfortunately none could be detected
Yoon, Soonsang. "Functional analysis of accessory proteins in equine infectious anaemia virus". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325550.
Texto completo da fonteHaziza, Brice. "Assemblage du lentivirus CAEV et approches vaccinales dans le modèle caprintitre". Aix-Marseille 2, 2000. http://www.theses.fr/2000AIX22033.
Texto completo da fontePrice, Amanda Jane. "Host-pathogen interactions in lentiviral post-entry restriction and nuclear import". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609671.
Texto completo da fonteMorin, Thierry. "Étude de l'évolution virologique et immunologique de l'infection par le virus de l'arthrite et de l'encéphalite caprine (CAEV) dans des modèles intra- et inter-spécifiques". Lyon 1, 2002. http://www.theses.fr/2002LYO10172.
Texto completo da fonteRousselot, Christian. "Préparation d'anticorps monoclonaux contre le virus Visna maedi et leurs applications". Lyon 1, 1989. http://www.theses.fr/1989LYO10041.
Texto completo da fonteQuillon, Aurélia. "Prédiction markovienne in silico des régions constantes et variables des lentivirus". Phd thesis, Université Claude Bernard - Lyon I, 2006. http://tel.archives-ouvertes.fr/tel-00124142.
Texto completo da fonteLisowski, Leszek. "Lentivirus-mediated globin gene transfer for the treatment of severe hemoglobinopathies /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528359391&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Texto completo da fonteQuillon, Aurélia Leroux Caroline Piau Didier. "Prédiction markovienne in silico des régions constantes et variables des lentivirus". [s.l.] : [s.n.], 2006. http://hal.archives-ouvertes.fr/docs/00/12/41/42/PDF/these_BoissinQuillon.pdf.
Texto completo da fonteBose, Deepanwita. "Tat-independent lentivirus genomes for vaccination and host/pathogen interaction studies". Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV009/document.
Texto completo da fonteOur lab has previously described the generation of a unique vaccine prototype against HIV-1/AIDS. It is a non-integrative DNA lentivector vaccine tested in pilot studies in animal models of HIV vaccine. The non-human primate study showed protection of all 6/6 macaques and immune response correlates were composed of a variety of effector (EM) and central memory (CM) T cells. More importantly, they also contained high proliferating antigen specific cells containing a type of stem cell-like memory T cells (TSCM). In this thesis the vaccine was enhanced further by switching the CXCR4 envelope of the vaccine to CCR5 tropic envelopes such as the clade B WARO obtained from a chronically infected patient and a series of three transmitted/founder (T/F) HIV Clade C strains from Zambia. To improve further the vaccine we developed new strategies to incorporate molecular adjuvants able to enhance and sustain the newly elicited immune responses.Since the human lentivirus HIV-1 has developed multiple complex strategies to persist, the focus of the next part of my thesis was to develop a tool to ease and better understand the underlying mechanisms of latency in infected memory CD4+ T cells. Latently-infected cells have non-expressed integrated viral DNA genomes. One of the main mechanisms of this latency is absence of Tat transactivation of the LTR promoter. The recent focus post development of efficient highly active antiviral therapy (HAART), is the cure of the reservoir of latently infected cells. One of the obstacles for this type of studies is the lack of proper primate lentivirus prototypes incapable of undergoing latency as extreme infection model in the evaluation. We hypothesized that a replication-competent SHIV genome driven by the Tat-independent constitutive-expression LTRs of CAEV will be a valuable tool for such studies. We designed chimeric CAEV LTRs bearing the attachment sequences of SIV at their extremities and used them to drive the complete genome of SHIV-KU2. The resulting construct is SHIV-YCC which is expected to generate virus that will not undergo latency due to absence of Tat. We found that cells transfected with SHIV-YCC genome produce SHIV proteins that are assembled into infectious particles released out of the cells. Virions are able to infect target CD4+ T cells both in primary PBMCs and cell lines. Passaged virus in macaques PBMCs increased virus replication and infectivity. SHIV-YCC is the first chimeric primate replication-competent lentivirus that constitutively expresses all viral proteins. This new model offers the possibility of studying the early events by which provirus undergoes latency particularly when the envelop gene will be replaced with that of the T/F CCR5 tropic HIV-1