Dissertations / Theses on the topic '(HIV-1)'
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Swan, Christina Heidi. "HIV-1 intracellular immunization via HIV-1 derived vector delivered genetic mechanisms." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3204640.
Full textTitle from first page of PDF file (viewed April 4, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Yang, Wa. "The evolution of HIV-1 and HIV-2." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405605.
Full textLeÌtourneau, Sven C. "HIV-1 vaccine development." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442825.
Full textHaddrick, Malcolm. "HIV-1 RNA dimerisation." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35383.
Full textDavis, Katie L. "Analysis of HIV-1 variable loop 3-specific neutralizing antibody responses by HIV-2/HIV-1 envelope chimeras." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/davis.pdf.
Full textDuvall, Melody Gayle. "HIV-specific cellular immune responses in HIV-1 and HIV-2 infection." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441307.
Full textMcIntyre, Glen J. Biotechnology & Biomolecular Sciences Faculty of Science UNSW. "Antiviral shRNA (for HIV-1)." Awarded by:University of New South Wales, 2006. http://handle.unsw.edu.au/1959.4/35215.
Full textArcher, John Patrick. "The diversity of HIV-1." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495044.
Full textBrown, D. E. "Antisense approaches towards HIV-1." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596956.
Full textHeap, Caroline J. "Analysis of HIV-1 neutralisation." Thesis, University of Warwick, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409953.
Full textRuggiero, Alessandra. "HIV-1 persistence during ART." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3003398/.
Full textMates, Jessica Marie. "TRANSCRIPTIONAL REGULATION OF HIV-1." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1395845500.
Full textSilva, Victor Barreto de Souza Brasil. "Co-infecção HIV-1/Tripanossomatídeos em macrófagos humanos efeito da infecção pelo HIV-1 e proteína Tat do HIV-1 sobre a replicação parasitária." reponame:Repositório Institucional da FIOCRUZ, 2009. https://www.arca.fiocruz.br/handle/icict/9114.
Full textFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Protozoários parasitos aparecem como co-patógenos em infecções pelo vírus da imunodeficiência humana (HIV)-1, resultando em um aumento mútuo na replicação viral e parasitária, e facilitando a progressão clínica de ambas as doenças. Os mecanismos pelos quais o HIV-1 induz um aumento na replicação do protozoário são desconhecidos. Neste trabalho, nós investigamos o papel do HIV-1 e da proteína trans-ativadora (Tat) do HIV-1 no aumento da replicação parasitária em macrófagos humanos primários co-infectados ou não com HIV-1 e Leishmania amazonensis ou com HIV-1 e Blastocrithidia culicis. Em alguns experimentos, macrófagos foram infectados somente com L. amazonensis ou B. culicis e expostos à proteína Tat recombinante do HIV-1. As replicações dos protozoários e do HIV-1 foram analisadas por índice endocítico ou ensaio imunoadsorvente ligado a enzima (ELISA) para p24, respectivamente. A infecção pelo HIV-1 dobrou a replicação da Leishmania em macrófagos, e soro contra o Tat do HIV-1 reduziu significativamente a replicação exacerbada do protozoário, indicando uma importante função desta proteína, a qual é liberada pelas células infectadas com HIV-1, neste processo. Corroborando estes resultados, a exposição de macrófagos infectados somente por Leishmania ao Tat recombinante (100 ng/mL) mimetizou a infecção pelo HIV-1. A multiplicação do protozoário diminuiu quando células infectadas por Leishmania foram tratadas com Tat na presença de anticorpos neutralizantes contra o Fator de Crescimento e Transformação (TGF)-b1, demonstrando a participação desta citocina no aumento da replicação da L. amazonensis em macrófagos. O tratamento com Tat induziu a expressão da enzima Ciclo-oxigenase (COX)-2 e a secreção de Prostaglandina E2 (PGE2), e o bloqueio da produção de PGE2 aboliu o aumento da replicação da Leishmania induzida por Tat Adição exógena de PGE2 estimulou o crescimento da Leishmania em macrófagos, e a neutralização imune de TGF-b1 abrandou este efeito. Analisados em conjunto, nós concluímos que Tat estimula a replicação da Leishmania via indução da síntese de PGE2 e conseqüentemente secreção de TGF-b1. Para avaliar se a infecção pelo HIV-1 desativa a atividade microbicida do macrófago, células infectadas com HIV-1 foram co-infectadas com um protozoário não patogênico (Blastocrithidia culicis), e nós observamos que a infecção pelo HIV-1 favoreceu a sobrevivência deste tripanossomatídeo. Por microscopia eletrônica, nós verificamos que tanto o HIV-1 quanto a B. culicis co-habitavam um mesmo macrófago, e que formas em divisão do protozoário podiam ser observadas no interior de macrófagos. De forma similar aos encontrados nos experimentos com Leishmania, o Tat ou o TGF-b1 dobraram o crescimento do protozoário em macrófagos infectados somente por Blastocrithidia. Em conclusão, nós identificamos, pela primeira vez, uma molécula do HIV-1 que promove a multiplicação de um protozoário patogênico (Leishmania), e permite a sobrevivência/crescimento em macrófagos humanos primários de um protozoário habitualmente não patogênico. Uma vez que a neutralização imune do Tat tem sido estudada como uma estratégia de vacinação contra o HIV-1, nossos resultados sugerem que a neutralização desta proteína também pode ser salutar no combate ao protozoário em casos de co-infecção
Protozoan parasites appear as human immunodeficiency virus (HIV)-1 co-pathogens, resulting in a mutuall enhancement of viral and parasite replication, and facilitating the clinical progression of both diseases. The mechanisms by which HIV-1 induces up-modulation of protozoan replication are unknown. In this work, we investigated the role of HIV-1 and HIV-1 transcriptional transactivator (Tat) protein in the enhancement of parasite replication in primary human macrophages co-infected or not with HIV-1. Human macrophages were co-infected with HIV-1 and either with Leishmania amazonensis or Blastocrithidia culicis. In selected assays, macrophages were infected only with L. amazonensis or B. culicis and exposed to recombinant HIV-1 Tat protein. Protozoan and HIV-1 replication were analyzed by endocytic index or p24 Enzyme Linked Immuno Sorbent Assay (ELISA), respectively. HIV-1 infection doubled the Leishmania replication in macrophages, and Tat antiserum significantly reduced the exacerbated parasite replication, pointing to a direct role of Tat protein released from HIV-1-infected cells in this process. Corroborating this finding, exposure of Leishmania-infected macrophages to recombinant Tat (100 ng/mL) mimicked HIV-1 infection. Protozoan replication diminished when Leishmania-infected cells were treated with Tat in the presence of neutralizing anti-Transforming Growth Factor (TGF)-b1 antibodies, showing a participation of this cytokine in the augmentation of L. amazonensis multiplication in macrophages. Interestingly, Tat induced the expression of the enzyme Cyclooxygenase (COX-2) and Prostaglandin E2 (PGE2) secretion, and blockage of PGE2 production abrogated the increased Leishmania replication induced by Tat. Exogenous addition of PGE2 elicited Leishmania replication in macrophages, and immunoneutralization of TGF-b1 blunted this effect. Taken together, we deciphered that Tat stimulates Leishmania replication via induction of PGE2 synthesis and consequently TGF-b1 secretion. To evaluate whether HIV-1 infection deactivates the microbicidal activity of macrophages, HIV- 1-infected cells were co-infected with a non-pathogenic protozoan (Blastocrithidia culicis), and we found that HIV-1 infection favors the survival of this trypanosomatid. By electron microscopy, we verify that both HIV-1 and B. culicis co-habited the same macrophage, and that dividing forms of the protozoan can be observed inside the macrophage. Similarly, Tat or TGF-b1 doubled the protozoan growth in Blastocrithidia-infected macrophages. In conclusion, we identified, for the first time, an HIV-1 molecule that promotes multiplication of a pathogenic protozoan (Leishmania) and permit survival of an otherwise non-pathogenic protozoan in primary human macrophages. Because immunoneutralization of HIV-1 Tat has been studied as a vaccination strategy against HIV-1, our results suggest that neutralization of this protein could be salutary in the combat against the protozoan in the cases of co-infection
Soto-Rifo, Ricardo. "Translational control of HIV-1 and HIV-2 genomic RNA." Lyon, Ecole normale supérieure, 2010. http://www.theses.fr/2010ENSL0584.
Full textInfections by Human immunodeficiency viruses type-1 and type-2 (HIV-1 and HIV-2) have an enormous impact in Human health as more than 33 million people is living with HIV/AIDS worldwide. The mechanisms controlling post-transcriptional events during the HIV life cycle have just started to capture the attention of scientists and most of the molecular processes allowing the genomic RNA to interact with the host machineries for translation, transport or decay are still obscure or in way to be determined. In this work, we contribute to the progress in the knowledge of the mechanisms controlling protein synthesis from the HIV-1 and HIV-2 genomic RNA. Results presented here provide evidence for the TAR RNA structure as a key player in controlling the interactions between the HIV-1 and HIV-2 genomic RNA with the host translational machinery. We also provide data for a new step during the HIV-2 life cycle that involves the accumulation of the genomic RNA in cytoplasmic granules containing several stress granules components. Finally, we present evidence for a potential mechanism by which nuclear export and protein synthesis are linked during the HIV-1 replication cycle. As such, we show that DEAD-box RNA helicase DDX3, previously implicated in Rev-mediated nuclear export, is absolutely required for HIV-1 genomic RNA translation. We determined the TAR structure as the viral determinant required for DDX3 function in translation. Strikingly, we also showed that DDX3 is specifically required for HIV-2 and SIV translation but not for FIV, HTLV-1, MLV or Line-1 suggesting that this function was acquired during primate lentiviruses evolution. Taken together, results obtained during this work highlight several key aspects of the HIV-1 and HIV-2 genomic RNA post-transcriptional control that may be critical for viral replication
Reinberger, Stefanie. "Phänotypische Charakterisierung des viralen Hüllproteins (Env) von HIV-1 durch Konstruktion rekombinanter HIV-1-Varianten." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964611155.
Full textWinstone, Nicola. "Characteristics of HIV-1 specific T cell responses in healthy, HIV-1 negative vaccine recipients." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491609.
Full textYilmaz, Alper. "Translational control of mRNAs transcribed from HIV-1 provirus and HIV-1 based lentiviral vectors." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1189785802.
Full textChen, H. K. Jonathan. "Molecular epidemiology of HIV-1 and characterization of drug resistant HIV-1 in Hong Kong." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634401.
Full textBates, Matthew Adam. "Betaherpesvirus genetic variation and infection in HIV-1 infected and 'HIV-1 exposed' Zambian children." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2010. http://researchonline.lshtm.ac.uk/4646542/.
Full textWang, Bin. "Molecular mechanisms in human immunodeficiency virus type-1 (HIV-1) pathogenesis and mother to child transmission of HIV-1." Thesis, The University of Sydney, 1996. https://hdl.handle.net/2123/27541.
Full textHan, Wenlong. "Interference with HIV-1 primer selection by siRNA directed to the HIV-1 primer binding site." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2006. https://www.mhsl.uab.edu/dt/2007r/han.pdf.
Full textRutbemberwa, Alleluiah. "Characterisation of HIV-1-Specific CD8+t Lymphocyte immune responses in HIV-1 infected Ugandan individuals." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289822.
Full textChen, Renxiang. "Studies of HIV-1 mutagenesis during drug therapy and the molecular determinants of HIV-1 variation." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1092663963.
Full textDocument formatted into pages. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Aug. 16.
Naghavi, Mojgan H. "Regulation of HIV-1 provirus transcription /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4865-8/.
Full textChen, Nan. "The role of HIV-1 Nef gene in HIV-mediated pathogenesis." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404289.
Full textWatkins, Gemma L. "A comparison of HIV-1 and HIV-2 gag gene expression." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/45902/.
Full textCleveland, S. Matthew. "HIV-1-specific antibody responses to a plant virus-HIV chimera." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340090.
Full textRocafort, Juncà Muntsa. "Gut microbiome in HIV-1 infection." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/666775.
Full textSoon after Human Immunodeficiency Virus type 1 (HIV-1) infection, a severe and rapid depletion of the gut-associated lymphoid tissue occurs, including significant loss of both, immune and epithelial host cells. This is followed by an increased permeability of the intestinal cell lining which facilitates microbial translocation. Microbial cells and products that are usually contained and controlled within the intestinal lumen, can now circulate in the bloodstream and become a new source for immune activation and inflammation. Because of the significant immune imbalance in the GALT after HIV-1 infection, recent microbiome research has focused on understanding the changes occurring in the microbial communities inhabiting the human gut after HIV-1 perturbation and in response to antiretroviral treatment (ART). Initial cross-sectional studies provided contradictory associations between gut microbial richness and diversity and HIV-1 infection and suggested shifts from Bacteroides to Prevotella predominance following viral infection. Nonetheless, these results have not been confirmed in animal models or in studies matched for HIV-1 transmission risk groups. For instance, in non-human primate models Simian Immunodeficiency Virus infection is followed by expansion of enteric virome but has a limited impact on the gut bacteriome. In two independent European cross-sectionals cohorts of chronically HIV-1-infected subjects and uninfected controls, in Barcelona (n=156) and Stockholm (n=84), men-who-have-sex-with-men (MSM) showed a Prevotella-enriched gut microbiota and higher microbial richness and diversity compared to non-MSM individuals who predominantly showed a Bacteroides-enriched microbiota, regardless of HIV-1 infection. After stratifying for sexual orientation (MSM vs. non-MSM), we described lower microbial richness and diversity in HIV-1 infected subjects, more so in subjects with an immune-discordant response to ART, but there was no solid evidence of an HIV-1-specific dysbiosis. In our Barcelona cohort, diet did not have a major impact on gut microbiota composition. To understand the longitudinal effects of HIV-1 infection on the human gut microbiota, we prospectively followed 49 Mozambican subjects diagnosed with recent HIV-1 infection and 54 uninfected controls for 9-18 months and compared them with 98 chronically HIV-1-infected subjects ART-treated (n=27) or not (n=71). Recent HIV-1infection was characterized by increased fecal Adenovirus shedding, which persisted during chronic HIV-1 infection and did not resolve with ART. Recent HIV-1 infection was also followed by transient non-HIV-1-specific changes in the gut bacterial richness and composition. Despite early resilience to change, an HIV-1-specific signature in the gut bacteriome could be eventually identified in chronically HIV-1-infected subjects. Such signature featured depletion of Akkermansia, Anaerovibrio, Bifidobacterium, and Clostridium, and has been previously associated with chronic inflammation, CD8+ T-cell anergy and metabolic disorders. In conclusion: 1) Sexual practice is an important confounding factor in microbiome studies that needs to be considered, especially in HIV-1-gut microbiota studies; 2) Gut microbiota is initially resilient to change right after HIV-1 acquisition but a pro-inflammatory-bacterial signature eventually appears in chronic phases of the infection, and 3) Changes on the gut microbiota do not only impact bacterial communities, but, at least, also viral communities.
Jauer, Christin Mariel. "Analyse eines unterquantifizierten HIV-1-Isolats." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-125031.
Full textGroot, Fedde. "Dendritic cell-mediated hiv-1 transmission." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2006. http://dare.uva.nl/document/36281.
Full textKjerrström, Zuber Anne. "Enhancement of HIV-1 DNA immunogens /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-304-x.
Full textAlaeus, Annette. "Significance of HIV-1 genetic subtypes /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3434-7/.
Full textEnting, Roeline Henny. "Neurological manifestations of HIV-1 infection." Rotterdam : Amsterdam : R.H.Enting ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/56445.
Full textBeerens, Nancy. "Regulation of HIV-1 reverse transcription." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/65252.
Full textAbdurahman, Samir. "Studies on HIV-1 core assembly /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-363-4/.
Full textSolis, Mayra. "Immune evasion mechanisms by HIV-1." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103531.
Full textL'induction de la réponse immunitaire innée par des pathogènes viraux est caractérisée par une production rapide des interférons de Type I (IFNβ/α). Les Toll-like (TLR) ou RIG-like (RLR) récepteurs détectent divers composants viraux induisant multiples voies de signalisation intracellulaire impliquées dans l'activation du factor de transcription-NF-B- ainsi que des facteurs de régulation de l'interféron-3 et -7 (IRF-3 et IRF-7). Ces évènements mènent à la synthèse de molécules immunorégulatrices, tel que les interférons (IFN) de Type I, les cytokines pro-inflammatoires et les gènes stimulés par l'IFN (ISG), qui jouent un rôle important dans l'inhibition de la réplication virale. Au cours de l'évolution, les virus ont développé des stratégies pour contrer la réponse immunitaire innée afin de se répliquer. Le virus de l'immunodéficience humaine de type 1(VIH-1), l'agent infectieux du syndrome de l'immunodéficience acquise (SIDA), échappe à la réponse immunitaire innée, ce qui favorise la progression de la maladie. Par conséquent, une meilleure compréhension des mécanismes par lesquels le VIH-1 module les voies de signalisation des TLR et des RLR pourrait mener au développement de nouvelles stratégies thérapeutiques pour empêcher la réplication et donc la propagation du VIH-1. Des études ont démontré que les TLR qui signalent par l'intermédiaire de NF-B augmentent la réplication du VIH-1. Cependant, la stimulation du TLR4 déclenche à la fois la voie de signalisation de NF-B et celle des IFN, pouvant avoir ainsi des effets inhibiteurs sur la réplication du VIH-1. L'objectif de notre première étude était de comprendre le rôle du TLR4 dans la réplication du VIH-1. Par conséquent, nous avons caractérisé la voie d'activation des IRF-3 et IRF-7 suite à la stimulation du TLR4. Nos résultats démontrent que les kinases non-canoniques TBK1et IKKε sont activées avec une cinétique distincte ayant pour conséquence l'activation de l'IRF-3 et l'induction subséquente des IFN de type I. Par conséquent, l'activation de la voie de signalisation des IFN par la stimulation du TLR4 pourrait offrir une nouvelle stratégie pour inhiber la réplication du VIH-1. Notre deuxième étude a eu pour but de définir les différentes voies de signalisation activées par le VIH-1. Les changements transcriptionels induits par les différents sous-types du VIH-1 dans les cellules dendritiques immatures ont été examinés par analyse de microréseaux. Nos résultats démontrent que pendant la phase tardive de l'infection VIH-1, un ensemble de gènes est différemment régulé par les différents sous-types du VIH-1. En plus, cette étude accentue le rôle important des cellules dendritiques immatures dans la réplication et la dissémination du VIH-1. En conclusion, étant donné l'importance des RLR dans la reconnaissance des virus à ARN, l'objectif de la dernière étude a été d'étudier les mécanismes d'évasion utilisés par VIH-1 pour contrer la réponse antivirale innée. Nos résultats démontrent que l'ARN du VIH-1 est détecté par le récepteur cytosolique RIG-I. Cependant, une protéine du VIH-1 -la protéase- séquestre le récepteur RIG-I dans les lysosomes et empêche l'activation de la réponse antivirale initié par le récepteur RIG-I. De façon générale, la recherche présentée dans cette thèse propose de nouvelles avenues pour développer des stratégies préventives et thérapeutiques afin de combattre le VIH-1/SIDA.
Chong, Sannie Siaw Foong. "Anisotropic potential HIV-1 protease inhibitors." Thesis, University of Hull, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327289.
Full textFiore, Simona. "HIV-1 infected women in Europe." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444410/.
Full textKong, Leopold. "HIV-1 gp120 : flexibility and glycosylation." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533859.
Full textKrashias, George. "Adjuvant for vaccination against HIV-1." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531970.
Full textForte, Serene E. "Envelope Determinants of HIV-1 Cytopathicity." eScholarship@UMMS, 1998. http://escholarship.umassmed.edu/gsbs_diss/190.
Full textMcClure, Charles Patrick. "HIV-1 in the genital tract." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275163.
Full textBristow, Richard G. W. "Antibody recognition of HIV-1 glycoproteins." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315370.
Full textMok, Hoi Ping. "Proviral gene expression of HIV-1." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614281.
Full textLockett, Sarah. "Factors affecting heterosexual HIV-1 transmission." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/12452.
Full textVigan, Raphael. "Cellular targets of HIV-1 VPU." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/cellular-targets-of-hiv1-vpu(14764437-266c-4b94-b53e-1a7a7e6ea2a9).html.
Full textChang, Jennifer Lynn. "Characterization of HIV-1 Rev mutants." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1363271761.
Full textWright, Alison Laing. "IGA MEDIATED DEFENSES AGAINST HIV-1." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1201290332.
Full textChinnadurai, Raghavan. "HIV-1 resistance to fusion inhibitors." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-58600.
Full textHermankova, Monika. "HIV-1 persistence under antiretroviral therapy." Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3080676.
Full text