Bibliografias temáticas / Lentivirusus

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Literatura científica selecionada sobre o tema "Lentivirusus"

Autor: Grafiati
Publicado: 25 de julho de 2024
Última modificação: 31 de julho de 2024

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Artigos de revistas sobre o assunto "Lentivirusus"

1

Clements, J. E., e M. C. Zink. "Molecular biology and pathogenesis of animal lentivirus infections." Clinical Microbiology Reviews 9, n.º 1 (janeiro de 1996): 100–117. http://dx.doi.org/10.1128/cmr.9.1.100.

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Lentiviruses are a subfamily of retroviruses that are characterized by long incubation periods between infection of the host and the manifestation of clinical disease. Human immunodeficiency virus type 1, the causative agent of AIDS, is the most widely studied lentivirus. However, the lentiviruses that infect sheep, goats, and horses were identified and studied prior to the emergence of human immunodeficiency virus type 1. These and other animal lentiviruses provide important systems in which to investigate the molecular pathogenesis of this family of viruses. This review will focus on two animal lentivirus models: the ovine lentivirus visna virus; and the simian lentivirus, simian immunodeficiency virus. These animal lentiviruses have been used to examine, in particular, the pathogenesis of lentivirus-induced central nervous system disease as models for humans with AIDS as well as other chronic diseases.
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2

Lairmore, M. D., S. T. Butera, G. N. Callahan e J. C. DeMartini. "Spontaneous interferon production by pulmonary leukocytes is associated with lentivirus-induced lymphoid interstitial pneumonia." Journal of Immunology 140, n.º 3 (1 de fevereiro de 1988): 779–85. http://dx.doi.org/10.4049/jimmunol.140.3.779.

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Abstract Ovine lentiviruses share genome sequence, structural features, and replicative mechanisms with HIV, the etiologic agent of AIDS. A lamb model of lentivirus-induced lymphoid interstitial pneumonia, comparable to lymphoid interstitial pneumonia associated with pediatric AIDS, was used to investigate production of leukocyte-soluble mediators. Lentivirus-infected lambs and adult sheep with severe lymphoid interstitial pneumonia had significantly elevated levels of spontaneous interferon (IFN) production from pulmonary leukocytes compared with ovine lentiviruses-infected animals with mild or no lesions of lymphoid interstitial pneumonia or non-infected controls. However, peripheral blood mononuclear cells from lentivirus-infected lambs did not spontaneously release significant amounts of IFN. IFN production by pulmonary lymph node lymphocytes was enhanced in the presence of lentivirus-infected alveolar macrophages. Animals with lentivirus-induced disease and spontaneous IFN production had enhanced virus replication within tissues. The ovine lentiviruses-induced IFN had a m.w. of between 25,000 and 35,000 and was resistant to freeze/thawing procedures. The IFN activity was sensitive to trypsin and stable to low pH and heat. IFN with similar physical and biochemical properties was produced when ovine lentiviruses was added to control leukocyte cultures. IL-2 and PGE2 production and responses to mitogen by pulmonary lymph node lymphocytes of lentivirus-diseased lambs were not statistically different from control animals. Increased local production of IFN in lentivirus-infected host tissues may serve to accelerate the entry of leukocytes into virus-induced lesions promoting cell-mediated tissue damage and also provide increased numbers of cells for virus replication.
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3

Hötzel, Isidro, e William P. Cheevers. "Conservation of Human Immunodeficiency Virus Type 1 gp120 Inner-Domain Sequences in Lentivirus and Type A and B Retrovirus Envelope Surface Glycoproteins". Journal of Virology 75, n.º 4 (15 de fevereiro de 2001): 2014–18. http://dx.doi.org/10.1128/jvi.75.4.2014-2018.2001.

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ABSTRACT We recently described a sequence similarity between the small ruminant lentivirus surface unit glycoprotein (SU) gp135 and the second conserved region (C2) of the primate lentivirus gp120 which indicates a structural similarity between gp135 and the inner proximal domain of the human immunodeficiency virus type 1 gp120 (I. Hötzel and W. P. Cheevers, Virus Res. 69:47–54, 2000). Here we found that the seven-amino-acid sequence of the gp120 strand β25 in the C5 region, which is also part of the inner proximal domain, was conserved in the SU of all lentiviruses in similar or identical positions relative to the carboxy terminus of SU. Sequences conforming to the gp135-gp120 consensus for β-strand 5 in the C2 region, which is antiparallel to β25, were then sought in the SU of other lentiviruses and retroviruses. Except for the feline immunodeficiency virus, sequences similar to the gp120-gp135 consensus for β5 and part of the preceding strand β4 were present in the SU of all lentiviruses. This motif was highly conserved among strains of each lentivirus and included a strictly conserved cysteine residue in β4. In addition, the β4/β5 consensus motif was also present in the conserved carboxy-terminal region of all type A and B retroviral envelope surface glycoproteins analyzed. Thus, the antiparallel β-strands 5 and 25 of gp120 form an SU surface highly conserved among the lentiviruses and at least partially conserved in the type A and B retroviral envelope glycoproteins.
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Armimi, Anastasia, Afina Firdaus Syuaib, Katherine Vanya, Marselina Irasonia Tan, Dessy Natalia, David Virya Chen, Chikako Ono, Yoshiharu Matsuura, Anita Artarini e Ernawati Arifin Giri-Rachman. "SARS-CoV-2 Neutralization Assay System using Pseudo-lentivirus". Indonesian Biomedical Journal 15, n.º 2 (18 de abril de 2023): 179–86. http://dx.doi.org/10.18585/inabj.v15i2.2212.

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BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects humans' lower respiratory tracts and causes coronavirus disease-2019 (COVID-19). Neutralizing antibodies is one of the adaptive immune system responses that can reduce SARS-CoV-2 infection. This study aimed to develop a SARS-CoV-2 neutralization assay system using pseudo-lentivirus.METHODS: The plasmid used for pseudo-lentivirus production was characterized using restriction analysis. The gene encoding for SARS-CoV-2 spike protein was confirmed using sequencing. The transfection pseudo-lentivirus optimal condition was determined by choosing the transfection reagents and adding centrifugation step. Optimal pseudo-lentivirus infection was analysed using fluorescent assay and luciferase assay. The optimal condition of pseudo-lentivirus infection was determined by the target cell type and the number of pseudo-lentiviruses used for neutralization test. SARS-CoV-2 pseudo-lentivirus was used to detect neutralizing antibodies from serum samples.RESULTS: The plasmid used for pseudo-lentivirus production was characterized and confirmed to have no mutations. Lipofectamine 2000 reagent generated pseudo-lentivirus with a higher ability to infect target cells, as indicated by a percentage green fluorescent protein (GFP) of 12.68%. Pseudo-lentivirus centrifuged obtained more stable results in luciferase expression. Optimal pseudo-lentivirus infection conditions were obtained using puromycin-selected HEK 293T-ACE2 cells as target cells. The number of pseudo-lentiviruses used in the neutralization assay system was multiplicity of infection (MOI) 0.075. Serum A samples with a 1:10 dilution had the highest neutralizing antibody activity.CONCLUSION: This study shows that SARS-CoV-2 neutralization assay system using pseudo-lentivirus successfully detected neutralizing antibodies in human serum, which were indicated by a decrease in the percentage of pseudo-lentivirus infections.KEYWORDS: COVID-19, neutralizing antibody, neutralization assay, pseudo-lentivirus, SARS-COV-2
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Courgnaud, Valérie, Xavier Pourrut, Frédéric Bibollet-Ruche, Eitel Mpoudi-Ngole, Anke Bourgeois, Eric Delaporte e Martine Peeters. "Characterization of a Novel Simian Immunodeficiency Virus from Guereza Colobus Monkeys (Colobus guereza) in Cameroon: a New Lineage in the Nonhuman Primate Lentivirus Family". Journal of Virology 75, n.º 2 (15 de janeiro de 2001): 857–66. http://dx.doi.org/10.1128/jvi.75.2.857-866.2001.

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ABSTRACT Exploration of the diversity among primate lentiviruses is necessary to elucidate the origins and evolution of immunodeficiency viruses. During a serological survey in Cameroon, we screened 25 wild-born guereza colobus monkeys (Colobus guereza) and identified 7 with HIV/SIV cross-reactive antibodies. In this study, we describe a novel lentivirus, named SIVcol, prevalent in guereza colobus monkeys. Genetic analysis revealed that SIVcol was very distinct from all other known SIV/HIV isolates, with average amino acid identities of 40% for Gag, 50% for Pol, 28% for Env, and around 25% for proteins encoded by five other genes. Phylogenetic analyses confirmed that SIVcol is genetically distinct from other previously characterized primate lentiviruses and clusters independently, forming a novel lineage, the sixth in the current classification.Cercopithecidae monkeys (Old World monkeys) are subdivided into two subfamilies, the Colobinae and theCercopithecinae, and, so far, allCercopithecidae monkeys from which lentiviruses have been isolated belong to the Cercopithecinae subfamily. Therefore, SIVcol from guereza colobus monkeys (C. guereza) is the first primate lentivirus identified in the Colobinaesubfamily and the divergence of SIVcol may reflect divergence of the host lineage.
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Browning, Matthew T., Russell D. Schmidt, Kathy A. Lew e Tahir A. Rizvi. "Primate and Feline Lentivirus Vector RNA Packaging and Propagation by Heterologous Lentivirus Virions". Journal of Virology 75, n.º 11 (1 de junho de 2001): 5129–40. http://dx.doi.org/10.1128/jvi.75.11.5129-5140.2001.

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ABSTRACT Development of safe and effective gene transfer systems is critical to the success of gene therapy protocols for human diseases. Currently, several primate lentivirus-based gene transfer systems, such as those based on human and simian immunodeficiency viruses (HIV/SIV), are being tested; however, their use in humans raises safety concerns, such as the generation of replication-competent viruses through recombination with related endogenous retroviruses or retrovirus-like elements. Due to the greater phylogenetic distance from primate lentiviruses, feline immunodeficiency virus (FIV) is becoming the lentivirus of choice for human gene transfer systems. However, the safety of FIV-based vector systems has not been tested experimentally. Since lentiviruses such as HIV-1 and SIV have been shown to cross-package their RNA genomes, we tested the ability of FIV RNA to get cross-packaged into primate lentivirus particles such as HIV-1 and SIV, as well as a nonlentiviral retrovirus such as Mason-Pfizer monkey virus (MPMV), and vice versa. Our results reveal that FIV RNA can be cross-packaged by primate lentivirus particles such as HIV-1 and SIV and vice versa; however, a nonlentivirus particle such as MPMV is unable to package FIV RNA. Interestingly, FIV particles can package MPMV RNA but cannot propagate the vector RNA further for other steps of the retrovirus life cycle. These findings reveal that diverse retroviruses are functionally more similar than originally thought and suggest that upon coinfection of the same host, cross- or copackaging may allow distinct retroviruses to generate chimeric variants with unknown pathogenic potential.
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Chen, Jianbo, Douglas Powell e Wei-Shau Hu. "High Frequency of Genetic Recombination Is a Common Feature of Primate Lentivirus Replication". Journal of Virology 80, n.º 19 (1 de outubro de 2006): 9651–58. http://dx.doi.org/10.1128/jvi.00936-06.

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ABSTRACT Recent studies indicate that human immunodeficiency virus type 1 (HIV-1) recombines at exceedingly high rates, approximately 1 order of magnitude more frequently than simple gammaretroviruses such as murine leukemia virus and spleen necrosis virus. We hypothesize that this high frequency of genetic recombination is a common feature of primate lentiviruses. Alternatively, it is possible that HIV-1 is unique among primate lentiviruses in possessing high recombination rates. Among other primate lentiviruses, only the molecular mechanisms of HIV-2 replication have been extensively studied. There are reported differences between the replication mechanisms of HIV-1 and those of HIV-2, such as preferences for RNA packaging in cis and properties of reverse transcriptase and RNase H activities. These biological disparities could lead to differences in recombination rates between the two viruses. Currently, HIV-1 is the only primate lentivirus in which recombination rates have been measured. To test our hypothesis, we established recombination systems to measure the recombination rates of two other primate lentiviruses, HIV-2 and simian immunodeficiency virus from African green monkeys (SIVagm), in one round of viral replication. We determined that, for markers separated by 588, 288, and 90 bp, HIV-2 recombined at rates of 7.4%, 5.5%, and 2.4%, respectively, whereas SIVagm recombined at rates of 7.8%, 5.6%, and 2.7%, respectively. These high recombination rates are within the same range as the previously measured HIV-1 recombination rates. Taken together, our results indicate that HIV-1, HIV-2, and SIVagm all possess high recombination frequencies; hence, the high recombination potential is most likely a common feature of primate lentivirus replication.
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Baccam, Prasith, Robert J. Thompson, Yuxing Li, Wendy O. Sparks, Michael Belshan, Karin S. Dorman, Yvonne Wannemuehler, J. Lindsay Oaks, James L. Cornette e Susan Carpenter. "Subpopulations of Equine Infectious Anemia Virus Rev Coexist In Vivo and Differ in Phenotype". Journal of Virology 77, n.º 22 (15 de novembro de 2003): 12122–31. http://dx.doi.org/10.1128/jvi.77.22.12122-12131.2003.

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ABSTRACT Lentiviruses exist in vivo as a population of related, nonidentical genotypes, commonly referred to as quasispecies. The quasispecies structure is characteristic of complex adaptive systems and contributes to the high rate of evolution in lentiviruses that confounds efforts to develop effective vaccines and antiviral therapies. Here, we describe analyses of genetic data from longitudinal studies of genetic variation in a lentivirus regulatory protein, Rev, over the course of disease in ponies experimentally infected with equine infectious anemia virus. As observed with other lentivirus data, the Rev variants exhibited a quasispecies character. Phylogenetic and partition analyses suggested that the Rev quasispecies comprised two distinct subpopulations that coexisted during infection. One subpopulation appeared to accumulate changes in a linear, time-dependent manner, while the other evolved radially from a common variant. Over time, the two subpopulations cycled in predominance coincident with changes in the disease state, suggesting that the two groups differed in selective advantage. Transient expression assays indicated the two populations differed significantly in Rev nuclear export activity. Chimeric proviral clones containing Rev genotypes representative of each population differed in rate and overall level of virus replication in vitro. The coexistence of genetically distinct viral subpopulations that differ in phenotype provides great adaptability to environmental changes within the infected host. A quasispecies model with multiple subpopulations may provide additional insight into the nature of lentivirus reservoirs and the evolution of antigenic and drug-resistant variants.
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Narayan, O., D. Sheffer, J. E. Clements e G. Tennekoon. "Restricted replication of lentiviruses. Visna viruses induce a unique interferon during interaction between lymphocytes and infected macrophages." Journal of Experimental Medicine 162, n.º 6 (1 de dezembro de 1985): 1954–69. http://dx.doi.org/10.1084/jem.162.6.1954.

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Lentivirus infections are characterized by a persistent, restricted type of virus replication in tissues. Using sheep and goat lentiviruses, whose target cells in vivo are macrophages, we explored virus-host cell interactions to determine whether an interferon (IFN) is produced during virus replication in vivo which causes restricted replication. We show that the lentiviruses were incapable of inducing IFN directly in any infected cell, including macrophages and lymphocytes. However, after infection with these viruses, sheep and goat macrophages acquired a factor that triggered IFN production by T lymphocytes. Only sheep/goat lentiviruses were capable of inducing the factor and, although these viruses replicated productively in various cell cultures of the natural host animal, only infected macrophages developed the IFN-inducing factor. The factor was produced continuously and was strictly cell associated, requiring direct contact with lymphocytes. The lymphocytes responded with a single, sudden release of IFN beginning 7 h after cocultivation and reaching peak values at 48 h, after which they ceased production and became refractory. IFN production was not immunologically specific and did not require histocompatibility between donors of the two cell types. The IFN is a nonglycosylated protein of molecular weight 54,000-64,000, and is stable to heat and acid treatments. These findings identify a unique IFN and a new method for virus induction of IFN. The novel two-stage process of induction provides a mechanism for local amplification and continuity of production of IFN in vivo. This is compatible with infection in the animal whose lentivirus-induced pathologic lesions consist of accumulations of lymphocytes and infected macrophages in target tissues.
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Kafri, Tal, Henriette van Praag, Ling Ouyang, Fred H. Gage e Inder M. Verma. "A Packaging Cell Line for Lentivirus Vectors". Journal of Virology 73, n.º 1 (1 de janeiro de 1999): 576–84. http://dx.doi.org/10.1128/jvi.73.1.576-584.1999.

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ABSTRACT Lentivirus vectors can transduce dividing and nondividing cells. Using three-plasmid transient transfections, high-titer (>109 IU/ml) recombinant lentivirus vectors pseudotyped with vesicular stomatitis virus G (VSV-G) protein can be generated (T. Kafri et al., Nat. Genet. 17:314–317, 1997; H. Miyoshi et al., Proc. Natl. Acad. Sci. USA 94:10319–10323, 1997; L. Naldini et al., Science 272:263–267, 1996). The recombinant lentiviruses can efficiently infect brain, liver, muscle, and retinal tissue in vivo. Furthermore, the transduced tissues demonstrated long-term expression of reporter genes in immunocompetent rodents. We now report the generation of a tetracycline-inducible VSV-G pseudotyped lentivirus packaging cell line which can generate virus particles at titers greater than 106 IU/ml for at least 3 to 4 days. The vector produced by the inducible cell line can be concentrated to titers of 109 IU/ml and can efficiently transduce nondividing cells in vitro and in vivo. The availability of a lentivirus packaging cell line will significantly facilitate the production of high-titer lentivirus vectors for gene therapy and study of human immunodeficiency virus biology.
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Mais fontes

Teses / dissertações sobre o assunto "Lentivirusus"

1

Robertson, David L. "Recombination in primate lentiviruses". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336866.

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Vödrös, Dalma. "Receptor use of primate lentiviruses /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-497-6/.

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Bailes, Elizabeth. "Origins and evolution of primate lentiviruses". Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246384.

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Cordeil, 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.

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Les IFN-I (interférons de type I), principalement IFN et , constituent un mécanisme de défense primordial de l’hôte contre les pathogènes. Pourtant, dans le cas du VIH-1 (virus de l’immunodéficience humaine), la relation entre les IFN-I et la réplication virale apparaît plus complexe. En effet, si les IFN-I inhibent la réplication du VIH-1 ex vivo, un état d’hyperactivation permanent de la réponse IFN-I a été récemment associé à la progression vers le SIDA ainsi qu’à une forte virémie chez les patients infectés par le VIH-1. De même, la dérégulation de la réponse IFN-I est un critère déterminant dans l’issue pathogénique de certains modèles d’infection virale chez le singe. Si l’hypothèse du rôle pathogénique des IFN-I s’avère correcte, le VIH-1 pourrait avoir évolué afin de se répliquer même en présence d’une telle réponse, qui semble être au final, plus délétère pour l’hôte que pour le virus. L’objectif de ce travail a été d’évaluer la résistance du VIH-1 aux IFN. Dans ce contexte, le VIH-1 a été comparé au VIH-2 et au SIVmac (virus de l’immunodéficience simienne), virus phylogénétiquement proches mais peu ou pas pathogènes pour l’homme, lors de l’infection de plusieurs types cellulaires tels que des lymphocytes, des macrophages et des cellules dendritiques. En accord avec l’hypothèse initiale de travail, les expériences réalisées ont montré que le VIH-1 est capable de se répliquer dans les cellules primaires prétraitées avec des doses d’IFN comparables à celles mesurées in vivo, alors que la réplication des virus VIH-2/SIVmac est complètement bloquée, même à des concentrations très faibles d’IFN. Ce travail a permis de démontrer que le blocage induit par l’IFN s’exerce au niveau des phases précoces de l’infection et plus précisément à l’étape de la transcription inverse. En effet, les données obtenues suggèrent que l’IFN induit l’expression d’un effecteur cellulaire qui affecte différentiellement la stabilité des complexes viraux, ce qui se traduit par un défaut d’accumulation de l’ADN viral plus important pour le VIH-2 et le SIVmac, que pour le VIH-1. La différence de susceptibilité des lentivirus de primates aux IFN-I pourrait ainsi expliquer en partie, les différents niveaux de réplication de ces virus, associés à leurs degrés de pathogénicité in vivo
Type 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
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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.

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Gene therapy is the introduction or alteration of genetic material with the intention to treat disease. To support this aim, viruses have been modified, with elements linked to viral pathogenicity removed from their genome and replaced by the genetic material to be delivered. Gene therapy vectors based on lentiviruses have many advantages, such as the ability to transduce non-dividing cells and to target specific cell types via pseudotyping. They have been successfully used in ex vivo clinical trials for several haematopoietic stem cell disorders. Lentiviral vectors, however, suffer from substantially lower titres than the more popular adeno-associated virus (AAV)-based vectors and therefore have limited applicability for in vivo gene therapy which requires much greater quantities of virus. The main aim of this thesis was to investigate strategies to improve lentiviral vector productivity during manufacture, in order to increase the likelihood of lentiviruses being adopted for disease treatment. Initial experiments were based on the lentiviral vector manufacturing process currently being developed by the United Kingdom Cystic Fibrosis Gene Therapy Consortium for the generation of highly concentrated, purified lentivirus for clinical use. Supplementation of FreeStyle 293 Expression Medium used during upstream processing was attempted, but none of the assessed supplements led to significant increases in lentiviral vector production. Investigation into intrinsic immunity to viral infection indicated that over-expression of the protein kinase RNA-activated (PKR) led to lower production titres, but over-expression of its inhibitors was not successful at increasing titres. The focus then shifted to reducing, or 'knocking-down', inhibitory factors present in the host cells, which could adversely affect viral titres. Investigation of the published HIV-1 literature revealed a possible 152 candidate inhibitory factors described as having a negative impact on HIV-1 replication in the late stages of the life cycle of the virus. A novel siRNA screen was developed to assess the effect of ‘knock-down' of inhibitory factors on lentiviral vector titre. Application of the screen to 89 candidate inhibitory factors identified nine genes which, when knocked-down, resulted in increased lentiviral vector production by more than 40%. Further work will be necessary to understand the role of the inhibitory factors in lentiviral vector production, but novel cell lines in which genes encoding these factors have been permanently deleted from producer cells could lead to higher titres, reducing costs in the manufacture of lentiviral vectors and making in vivo gene therapy more feasible from a health economics perspective.
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Kelly, 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.

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Martin, 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.

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Les VIH-1 et VIH-2, lentivirus responsables du SIDA, sont issus de transmissions inter-espèces de virus simiens (SIV) à l'homme. Outre leurs protéines de structure et de régulation, les lentivirus codent pour des protéines auxiliaires qui favorisent la réplication virale dans la cellule hôte en contrecarrant des facteurs cellulaires antiviraux, appelés facteurs de restriction. Le mécanisme d'action de ces protéines virales auxiliaires repose souvent sur le détournement de complexes Ubiquitine-Ligases, un mécanisme très répandu chez une grande variété de pathogènes, en vue de dégrader des protéines de la cellule hôte. Ce mécanisme est utilisé par la protéine Vpx, exprimée uniquement par VIH-2 (et non par VIH-1), qui induit la dégradation de SAMDH1, un facteur de restriction bloquant l'étape de transcription inverse. Ainsi, Vpx fait un pont moléculaire entre l'adaptateur DCAF1 du complexe Ubiquitine-Ligase Cul4A-DDB1(DCAF1) et SAMHD1, ce qui entraîne l'ubiquitination et la dégradation de SAMHD1. En 2018, notre équipe a montré que Vpx induisait la dégradation d'un facteur cellulaire supplémentaire : le complexe HUSH, composé de TASOR, MPP8 et Périphiline. Ce complexe intervient dans la répression épigénétique non seulement de nombreux gènes cellulaires, d'éléments rétro-transposables et de rétrovirus endogènes, mais aussi du génome du VIH intégré dans celui de la cellule infectée. En dégradant HUSH, Vpx favorise l'expression virale. Dans ce contexte, les objectifs de ma thèse ont été de : (i) Déterminer si le mécanisme de dégradation de HUSH induit par Vpx de VIH2 était identique au mécanisme de dégradation de SAMHD1. J'ai pu mettre en évidence des différences importantes entre les deux mécanismes bien que Vpx utilise, dans les deux cas, le même adaptateur d'Ubiquitine-Ligase, DCAF1 (coeur principal du travail de thèse, article soumis). (ii) Caractériser les déterminants moléculaires en jeu dans l'antagonisme de HUSH par d'autres protéines lentivirales. Premièrement, il s'agissait de savoir si les différentes protéines virales apparentées à Vpx chez différentes espèces de virus simiens avaient toutes la même capacité à dégrader le complexe HUSH. Nous avons ainsi pu mettre en évidence une spécificité lentivirale de l'antagonisme du complexe HUSH, une caractéristique majeure des facteurs de restriction (contribution à l'article Chougui et al., Nature microbiology, 2018). Dans un second temps, ceci m'a conduit à débuter l'étude des déterminants viraux de ces protéines apparentées à Vpx, telles les protéines Vpr de différentes souches de SIVagm (infectant le singe vert africain) qui présentent des phénotypes différents quant à la dégradation de SAMHD1 ou de HUSH (travail en cours). L'ensemble des résultats a permis, d'une part de mieux caractériser le mécanisme d'antagonisme de HUSH par les protéines lentivirales Vpx/Vpr, et d'autre part de fournir de premiers outils moléculaires pour différencier l'antagonisme de HUSH de celui de SAMHD1 dans les cellules primaires. Dans le futur, les données pourront aider à mieux comprendre comment diverses protéines lentivirales se sont adaptées à leurs différents substrats cellulaires (et vice-versa) au cours de l'évolution. Enfin, cibler HUSH grâce à l'identification de déterminant d'interaction ou de dégradation pourrait être intéressant pour le développement de nouvelles cibles thérapeutiques
HIV-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
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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.

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Lentiviruses have paradoxically fast short-term rate of evolution and slow long-term rate of evolution, which differ by several orders of magnitude. In this thesis, with a new method called truncated tree analysis, slower rates of evolution of transmitted viruses were estimated. However, the rate decline of the transmitted viruses is limited, and is not sufficient to explain the dramatic difference between the short-term and long-term evolutionary rates. These dramatically different rates were reconciled by an S shaped curve based on the new trend observed from this thesis. In the middle part of this new trend, the rate of evolution decreases as the time of divergence increases. Using this new trend, the time scale of HIV -1 and their closest related SIV found in apes were set. The SIV cpzPtt and SIV cpzPts isolated from the two subspecies of chimpanzees shared the most recent common ancestor around 25.2 thousand years ago. This is younger than the estimated date of these two host subspecies split, and suggests that the SIV cpz is relatively new to the chimpanzees. The second chapter of this thesis further explores lentiviral evolution by examining the feline immunodeficiency viruses (FIV's). An American origin scenario of the FIV s was proposed. In this scenario the ancestor of FIV first the invaded the ancestors of the puma lineage living in American, and then as the ancient puma lineage speciated and migrated FIV spread out to many other felids. The final chapter of this thesis further explores the evolutionary rate decline as the time span extends by introducing the idea of flip- flop sites that undergo negative frequency dependent selection pressures. Theoretical simulations confirmed that in the short time span, the presence of the flip-flop sites results in overestimation of the evolutionary rate, but in longer time spans, opposite effects of flip-flop sites were observed.
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Lee, Wei-Cheng. "Studies on lentivirus infection of macrophages". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/29845.

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Several aspects of the interaction of macrophages and maedi visna virus (MVV) were undertaken: viral replication, phenotype, phagocytosis and antigen presenting function of macrophages after MVV (EV1) infection. MVV replication in monocyte-derived-macrophages (MDM) showed viral budding sites both at cytoplasmic and vesicular membranes. In contrast, viral budding sites predominantly occurred at the cytoplasmic membrane of skin fibroblasts, whilst virus accumulated in vesicular lumens of MVV-infected alveolar macrophages (AM). Many intracytoplasmic type A (ICA) particles accumulated in the cytoplasm of MDM and AM infected with EV1. Expression of MHC class II, MHC class I, CD4, CD8, LFA-1 and VPM32 antigen on MDM infected in vitro was unaltered by 5 days after MVV infection (P>0.05). In vivo MHC class I, class II (DQ & DR) and LFA-1 expression on AM from MVV infected sheep with lung lesions was greatly increased to uninfected sheep (P<0.05). A significant decrease in the CD4:CD8 ratio in bronchoalveolar lymphocytes was also found in the same group. The phagocytic activity of macrophages after MVV infection was also studied both in vivo and in vitro. There was a decrease in the phagocytic activity for RBC (P<0.05) and yeast by MVV-infected MDM after 5 days post infection, but the FcR expression of MDM assayed by erythrocyte rosetting (ER) did not show a significant difference between MVV and mock infected MDM. In vivo, there was no significant difference in ER, phagocytosis of RBC and P. hemolytica by monocytes between MVV-infected and control sheep. However surface binding and phagocytosis of opsonized P. hemolytica by AM from MVV infected sheep without lung lesions was significantly increased compared to uninfected sheep (P<0.05), but this increase was not seen in ER and phagocytosis of RBC by AM in the same group. In contrast the ER, phagocytosis of RBC and P. hemolytica by AM from sheep with lung lesions was slightly lower, but not significantly different from uninfected sheep.
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Starling, Isabella. "Mechanisms and specificity of lentivirus neurotoxicity". Thesis, University of Edinburgh, 1998. http://webex.lib.ed.ac.uk/abstracts/starli01.pdf.

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Livros sobre o assunto "Lentivirusus"

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Maurizio, Federico, ed. Lentivirus gene engineering protocols. Totowa, N.J: Humana Press, 2003.

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missing], [name. Lentivirus gene engineering protocols. Totowa, NJ: Humana Press, 2003.

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Maurizio, Federico, ed. Lentivirus gene engineering protocols. 2a ed. New York: Humana Press, 2010.

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Federico, Maurizio, ed. Lentivirus Gene Engineering Protocols. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1592593933.

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Federico, Maurizio, ed. Lentivirus Gene Engineering Protocols. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-533-0.

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E, Wilcox G., Soeharsono S, Dharma D. M. N, Copland J. W, AustralianCentre for International Agricultural Research., Indonesia Direktorat Jenderal Petermakan e Bali Cattle Disease Investigation Unit., eds. Jembrana disease and the bovine lentiviruses: Proceedings of a workshop 10-13 June 1996, Bali, Indonesia. Canberra: Australian Centre for International Agricultural Research in association with Direktorat Jenderal Petermakan and the Bali Cattle Disease Investigation Unit, 1997.

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7

Milne, Catherine E. Maedi visna: The disease, its potential impact on the UK sheep industry and a cost benefit appraisal ofcontrol strategies. [Aberdeen]: SAC, 1993.

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1949-, Morrow John, e Haigwood Nancy L, eds. HIV molecular organization, pathogenicity, and treatment. Amsterdam: Elsevier, 1993.

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1963-, Sobo Elisa Janine, ed. The endangered self: Managing the social risk of HIV. London: Routledge, 2000.

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Nichols, Eve K. Expanding access to investigational therapies for HIV infection and AIDS: March 12-13, 1990, conference summary. Washington, D.C: National Academy Press, 1991.

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Capítulos de livros sobre o assunto "Lentivirusus"

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Federico, Maurizio. "From Lentiviruses to Lentivirus Vectors". In Lentivirus Gene Engineering Protocols, 3–15. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1-59259-393-3:3.

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Lu, Yichen, e Max Essex. "Lentivirus‡". In The Springer Index of Viruses, 1693–702. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-95919-1_275.

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Gonda, Matthew A. "The Lentiviruses of Cattle". In The Retroviridae, 83–109. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1730-0_3.

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Planelles, Vicente. "Hybrid Lentivirus Vectors". In Lentivirus Gene Engineering Protocols, 273–84. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1-59259-393-3:273.

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Surdziel, Ewa, Matthias Eder e Michaela Scherr. "Lentivirus-Mediated Antagomir Expression". In Methods in Molecular Biology, 237–48. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-811-9_16.

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Fultz, P. N. "SIVsmmPBj14: An Atypical Lentivirus". In Current Topics in Microbiology and Immunology, 65–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78536-8_4.

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Zhao, Jing, e Andrew M. L. Lever. "Lentivirus-Mediated Gene Expression". In Methods in Molecular Biology, 343–55. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-030-0_20.

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Benskey, Matthew J., e Fredric P. Manfredsson. "Lentivirus Production and Purification". In Gene Therapy for Neurological Disorders, 107–14. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3271-9_8.

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Dreyer, Jean-Luc. "Lentiviral Vector-Mediated Gene Transfer and RNA Silencing Technology in Neuronal Dysfunctions". In Lentivirus Gene Engineering Protocols, 3–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-533-0_1.

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Coppola, Valeria, Cesare Galli, Maria Musumeci e Désirée Bonci. "Manipulating the Cell Differentiation Through Lentiviral Vectors". In Lentivirus Gene Engineering Protocols, 149–60. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-533-0_10.

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Trabalhos de conferências sobre o assunto "Lentivirusus"

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Xiao, Yun-Feng. "Label-free Detection of Single Nanoparticles and Lentiviruses Using an Optical Microcavity". In Optical Sensors. Washington, D.C.: OSA, 2013. http://dx.doi.org/10.1364/sensors.2013.st2b.3.

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Hoffman, Robert M., Hiroyuki Kishimoto e Toshiyoshi Fujiwara. "Specific in vivo labeling with GFP retroviruses, lentiviruses, and adenoviruses for imaging". In Biomedical Optics (BiOS) 2008, editado por Alexander P. Savitsky, Robert E. Campbell e Robert M. Hoffman. SPIE, 2008. http://dx.doi.org/10.1117/12.773308.

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Tulio, Robertha, e Rômulo Machado Balmant. "Dental care for HIV positive patients - care and importance - case report". In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-087.

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Abstract Acquired immunodeficiency syndrome (AIDS) is caused by the "Lentivirus" family of retroviruses, called HIV-1. This syndrome is defined as an infectious disease of viral origin, with its manifestation interspersed in peaks and troughs, with a pathophysiology involving the compromising of the immune system, causing the defense system to not operate correctly, leaving the patient susceptible to the development of infections.
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Tapanes-Castillo, Alexis, Derek Dykxhoorn, Leana Ramos, Milagros Mulero, Deliabell Hernandez e Vadym Trokhymchuk. "Culturing Human Neural Stem Cells and Quantifying Lentiviruses to Study Autism." In MOL2NET 2016, International Conference on Multidisciplinary Sciences, 2nd edition. Basel, Switzerland: MDPI, 2016. http://dx.doi.org/10.3390/mol2net-02-07008.

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Alton, EWFW, AC Boyd, JC Davies, DR Gill, U. Griesenbach, TE Harman, SC Hyde e G. McLachlan. "S68 Towards a first-in-human trial with a pseudotyped lentivirus". In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.73.

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Lund-Palau, H., C. Meng, A. Pilou, N. Atsumi, A. Bhargava, M. Chan, A. Byrne et al. "T2 Lentivirus GM-CSF gene therapy ameliorates autoimmune pulmonary alveolar proteinosis". In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.2.

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Burke, David, Kristine Drafahl, Clark Fjeld, Chad Galderisi e Cindy Spittle. "Abstract 896: Enhanced sensitivity detection of replication competent lentivirus by qPCR". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-896.

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Wilson, AA, GJ Murphy, H. Hamakawa, L. Kwok, S. Srinivasan, A. Hovav, RC Mulligan, S. Amar, B. Suki e DN Kotton. "Lentivirus-Based Expression of Human Alpha-1 Antitrypsin Ameliorates Emphysema in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3509.

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Marcotte, Richard, Azin Sayad, Maliha Haider, Kevin Brown, Troy Ketela, Jason Moffat e Benjamin G. Neel. "Abstract PR01: Functional characterization of breast cancer using pooled lentivirus shRNA screens". In Abstracts: AACR Precision Medicine Series: Synthetic Lethal Approaches to Cancer Vulnerabilities - May 17-20, 2013; Bellevue, WA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.pms-pr01.

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Marcotte, Richard, Kevin Brown, Azin Sayad, Maliha Haider, Troy Ketela, Jason Moffat e Benjamin G. Neel. "Abstract 5084: Functional genomic classification of breast cancer using pooled lentivirus shRNA screens". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5084.

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Relatórios de organizações sobre o assunto "Lentivirusus"

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Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, julho de 2012. http://dx.doi.org/10.21236/ada566912.

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Lindner, Daniel J. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, janeiro de 2013. http://dx.doi.org/10.21236/ada581503.

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Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, julho de 2011. http://dx.doi.org/10.21236/ada581646.

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DeMartini, James C., Abraham Yaniv, Jonathan O. Carlson, Arnona Gazit, Leonard E. Pearson, Kalman Perk, J. K. Young, Noam Safran e A. Friedman. Evaluation of Naked Proviral DNA as a Vaccine for Ovine Lentivirus Infection. United States Department of Agriculture, setembro de 1994. http://dx.doi.org/10.32747/1994.7570553.bard.

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Ovine lentivirus (OvLV) infection is widespread in sheep of the United States and Israel and is responsible for substantial economic losses. The primary goal of this project was to evaluate naked proviral DNA as a vaccine to induce protective immunity in sheep in endemic areas. Contrary to expectations, inoculation of sheep with proviral DNA derived from the full length OvLV molecular clone pkv72 did not result in detectable OvLV infection, but infectious virus was recovered from transfected ovine cells. Kv72 virus produced by these cells infected sheep and induced antibody responses, and was used as a viral challenge in subsequent experiments. To improve in vivo transfection efficiency and compare the viral LTR with other romoters, expression of reporter genes was studied in sheep transfected in vivo by injection of cationic liposome-DNA complexes; one formulation produced gene expression in a sheep for 4 months following a single intravenous injection. Since the pol-deleted OvLV construct was not stable in vivo, twelve lambs were injected with plasmids containing the Kv72 gag region (pCMVgag) or env region (pCMVenv), or saline. Prior to challenge, no detectable anti-OvLV immune responses were detected. Following homologous challenge with OvLV. Although the naked DNA approach to vaccination holds promise for control of ovine lentivirus-induced disease, further work needs to be done to develop more effective methods of transfecting sheep with DNA.
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