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Bibliografías temáticas / HIV-1 infectivity

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Literatura académica sobre el tema "HIV-1 infectivity"

Autor: Grafiati

Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "HIV-1 infectivity"

1

Fox, Philip C., Andy Wolff, Chih-Ko Yeh, Jane C. Atkinson y Bruce J. Baum. "Saliva inhibits HIV-1 infectivity". Journal of the American Dental Association 116, n.º 6 (mayo de 1988): 635–37. http://dx.doi.org/10.14219/jada.archive.1988.0002.

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Maeda, Yosuke, Keisuke Yusa y Shinji Harada. "Enhanced infectivity of HIV-1 by X4 HIV-1 coinfection". Biochemical and Biophysical Research Communications 308, n.º 4 (septiembre de 2003): 906–13. http://dx.doi.org/10.1016/s0006-291x(03)01498-0.

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Hood, Joshua L., Andrew P. Jallouk, Nancy Campbell, Lee Ratner y Samuel A. Wickline. "Cytolytic nanoparticles attenuate HIV-1 infectivity". Antiviral Therapy 18, n.º 1 (2012): 95–103. http://dx.doi.org/10.3851/imp2346.

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Jones, Jennifer, William Whitford, Frederic Wagner y Olaf Kutsch. "Optimization of HIV-1 infectivity assays". BioTechniques 43, n.º 5 (noviembre de 2007): 589–94. http://dx.doi.org/10.2144/000112624.

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HAMMAR, LENA, IVAN HIRSCH, ALCYONE MACHADO, JEAN MAREUIL, JEAN BAILLON y JEAN-CLAUDE CHERMANN. "Lectin Effects on HIV-1 Infectivity". Annals of the New York Academy of Sciences 724, n.º 1 Slow Infectio (mayo de 1994): 166–69. http://dx.doi.org/10.1111/j.1749-6632.1994.tb38907.x.

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Zhang, Jianyong y Chen Liang. "BST-2 Diminishes HIV-1 Infectivity". Journal of Virology 84, n.º 23 (22 de septiembre de 2010): 12336–43. http://dx.doi.org/10.1128/jvi.01228-10.

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ABSTRACT Bone marrow stromal cell antigen 2 (BST-2, also known as tetherin/CD317/HM1.24) inhibits the release of human immunodeficiency virus type 1 (HIV-1) and other enveloped viruses by tethering virus particles to the cell surface. In this study, we provide evidence not only that the yield of cell-free HIV-1 particles is significantly reduced by BST-2 but also that the infectivity of these progeny virions is severely impaired. The lowered virion infectivity is due to the accumulation of pr55 Gag precursor and the p40Gag intermediates as well as to the loss of a mature core in the majority of HIV-1 particles. These data suggest that, in addition to impeding the release of HIV-1 particles from host cells, BST-2 may also interfere with the activation of viral protease and, as a result, impairs viral Gag processing as well as maturation of HIV-1 particles.

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7

Konopka, K., B. R. Davis, C. E. Larsen y N. Düzgünes. "Cardiolipin liposomes specifically inhibit HIV-1 infectivity". Antiviral Research 15 (abril de 1991): 68. http://dx.doi.org/10.1016/0166-3542(91)90131-a.

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Rapatski, Brandy L., Frederick Suppe y James A. Yorke. "Reconciling Different Infectivity Estimates for HIV-1". JAIDS Journal of Acquired Immune Deficiency Syndromes 43, n.º 3 (noviembre de 2006): 253–56. http://dx.doi.org/10.1097/01.qai.0000243095.19405.5c.

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Müller, Barbara, Maria Anders, Hisashi Akiyama, Sonja Welsch, Bärbel Glass, Krisztina Nikovics, Francois Clavel, Hanna-Mari Tervo, Oliver T. Keppler y Hans-Georg Kräusslich. "HIV-1 Gag Processing Intermediates Trans-dominantly Interfere with HIV-1 Infectivity". Journal of Biological Chemistry 284, n.º 43 (7 de agosto de 2009): 29692–703. http://dx.doi.org/10.1074/jbc.m109.027144.

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Crombie, René, Roy L. Silverstein, Clarinda MacLow, S. Frieda A. Pearce, Ralph L. Nachman y Jeffrey Laurence. "Identification of a CD36-related Thrombospondin 1–binding Domain in HIV-1 Envelope Glycoprotein gp120: Relationship to HIV-1–specific Inhibitory Factors in Human Saliva". Journal of Experimental Medicine 187, n.º 1 (5 de enero de 1998): 25–35. http://dx.doi.org/10.1084/jem.187.1.25.

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Human and non–human primate salivas retard the infectivity of HIV-1 in vitro and in vivo. Because thrombospondin 1 (TSP1), a high molecular weight trimeric glycoprotein, is concentrated in saliva and can inhibit the infectivity of diverse pathogens in vitro, we sought to determine the role of TSP1 in suppression of HIV infectivity. Sequence analysis revealed a TSP1 recognition motif, previously defined for the CD36 gene family of cell adhesion receptors, in conserved regions flanking the disulfide-linked cysteine residues of the V3 loop of HIV envelope glycoprotein gp120, important for HIV binding to its high affinity cellular receptor CD4. Using solid-phase in vitro binding assays, we demonstrate direct binding of radiolabeled TSP1 to immobilized recombinant gp120. Based on peptide blocking experiments, the TSP1–gp120 interaction involves CSVTCG sequences in the type 1 properdin-like repeats of TSP1, the known binding site for CD36. TSP1 and fusion proteins derived from CD36-related TSP1-binding domains were able to compete with radiolabeled soluble CD4 binding to immobilized gp120. In parallel, purified TSP1 inhibited HIV-1 infection of peripheral blood mononuclear cells and transformed T and promonocytic cell lines. Levels of TSP1 required for both viral aggregation and direct blockade of HIV-1 infection were physiologic, and affinity depletion of salivary TSP1 abrogated >70% of the inhibitory effect of whole saliva on HIV infectivity. Characterization of TSP1–gp120 binding specificity suggests a mechanism for direct blockade of HIV infectivity that might be exploited to retard HIV transmission that occurs via mucosal routes.

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Tesis sobre el tema "HIV-1 infectivity"

1

Walker, Polly Rose. "Evolution and infectivity of HIV-1 subtype C viruses". Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442985.

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Newman, Edmund Nicholas. "Genetic and functional analysis of APOBEC3G : a suppressor of HIV-1 infectivity". Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428527.

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3

Auclair, Jared R. "Probing the Structural Topology of HIV-1 Virion Infectivity Factor (VIF): A Dissertation". eScholarship@UMMS, 2012. http://escholarship.umassmed.edu/gsbs_diss/359.

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Human Immunodeficiency Virus Type 1 (HIV-1), the virus that causes Acquired Immunodeficiency Syndrome (AIDS), attacks the immune system leaving patients susceptible to opportunistic infections that eventually cause death. Highly Active Antiretroviral Therapy, HAART, is the current drug strategy used to combat HIV. It is a combination therapy that includes HIV-1 Reverse Transcriptase and HIV-1 Protease inhibitors. Drug resistant strains arise that evade current HAART treatments; therefore novel drugs are needed. HIV-1 regulatory proteins such as Tat, Rev, Nef, Vpr, Vpu, and Vif are attractive new drug targets. Of particular interest is the HIV-1 Vif protein and its cellular binding partner APOBEC3G. In the absence of HIV-1 Vif, APOBEC3G, a cytidine deaminase, is able to mutate the viral cDNA and render the virus noninfectious. HIV-1 Vif binds to APOBEC3G and targets it for proteosomal degradation through an interaction with a Cullin-RING ligase complex. Blocking the HIV-1 Vif APOBEC3G interaction would allow APOBEC3G to perform its antiviral function. An attractive strategy to target the HIV-1 Vif APOBEC3G interaction would be a structure-based one. To apply structure-based drug design approaches to HIV-1 Vif and APOBEC3G, I attempted to collect high resolution structural data on HIV-1 Vif and APOBEC3G. My attempts were unsuccessful because the milligram quantities of soluble protein required were not obtained. Therefore, in Chapter III I used chemical cross-linking and mass spectrometry to probe the structural topology of HIV-1 Vif obtaining low resolution structural data. Chemical cross-linking formed HIV-1 Vif multimers including dimers, trimers, and tetramers. Analysis of the cross-linked monomer revealed that HIV-1 Vif’s N-terminal domain is a well-folded, compact, globular domain, where as the C-teriminal domain is predicted to be disordered. In addition, disorder prediction programs predicted the C-terminal domain of HIV-1 Vif to be disordered. Upon oligomerization the C-terminal domain undergoes a disorder-to-order transition that not only facilitates oligomerization but may facilitate other protein-protein interactions. In addition, HIV-1 Vif oligomerization bring Lys34 and Glu134 in close proximity to each other likely creating one molecular surface forming a “hot spot” of biological activity. In Chapter IV I confirmed my low resolution structural data via peptide competition experiments where I identified peptides that can be used as scaffolds for future drug design. HIV-1 Vif oligomerization is concentration dependent. The HIV-1 Vif peptides Vif(29-43) and Vif(125-139) were able to disrupt HIV-1 Vif oligomerization, which confirms the low resolution structural data. HIV-1 Vif peptides Vif(25-39) and Vif(29-43) reduced the amount of APOBEC3G immobilized on the Protein A beads, reduced the amount of HIV-1 Vif interacting with APOBEC3G, or degraded APOBEC3G itself. These peptides could be used as scaffolds to design novel drugs that disrupt the function of HIV-1 Vif and or APOBEC3G. Therefore, low resolution structural data and peptide competition experiments were successful in identifying structurally important domains in HIV-1 Vif. They also provided insight into a possible mechanism for HIV-1 Vif function where a disorder-to-order transition facilitates HIV-1 Vif’s ability to interact with a diverse set of macromolecules. These data advance our structural understanding of HIV-1 Vif and they will facilitate future highresolution studies and novel drug designs.

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4

Auclair, Jared R. "Probing the Structural Topology of HIV-1 Virion Infectivity Factor (VIF): A Dissertation". eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/359.

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Human Immunodeficiency Virus Type 1 (HIV-1), the virus that causes Acquired Immunodeficiency Syndrome (AIDS), attacks the immune system leaving patients susceptible to opportunistic infections that eventually cause death. Highly Active Antiretroviral Therapy, HAART, is the current drug strategy used to combat HIV. It is a combination therapy that includes HIV-1 Reverse Transcriptase and HIV-1 Protease inhibitors. Drug resistant strains arise that evade current HAART treatments; therefore novel drugs are needed. HIV-1 regulatory proteins such as Tat, Rev, Nef, Vpr, Vpu, and Vif are attractive new drug targets. Of particular interest is the HIV-1 Vif protein and its cellular binding partner APOBEC3G. In the absence of HIV-1 Vif, APOBEC3G, a cytidine deaminase, is able to mutate the viral cDNA and render the virus noninfectious. HIV-1 Vif binds to APOBEC3G and targets it for proteosomal degradation through an interaction with a Cullin-RING ligase complex. Blocking the HIV-1 Vif APOBEC3G interaction would allow APOBEC3G to perform its antiviral function. An attractive strategy to target the HIV-1 Vif APOBEC3G interaction would be a structure-based one. To apply structure-based drug design approaches to HIV-1 Vif and APOBEC3G, I attempted to collect high resolution structural data on HIV-1 Vif and APOBEC3G. My attempts were unsuccessful because the milligram quantities of soluble protein required were not obtained. Therefore, in Chapter III I used chemical cross-linking and mass spectrometry to probe the structural topology of HIV-1 Vif obtaining low resolution structural data. Chemical cross-linking formed HIV-1 Vif multimers including dimers, trimers, and tetramers. Analysis of the cross-linked monomer revealed that HIV-1 Vif’s N-terminal domain is a well-folded, compact, globular domain, where as the C-teriminal domain is predicted to be disordered. In addition, disorder prediction programs predicted the C-terminal domain of HIV-1 Vif to be disordered. Upon oligomerization the C-terminal domain undergoes a disorder-to-order transition that not only facilitates oligomerization but may facilitate other protein-protein interactions. In addition, HIV-1 Vif oligomerization bring Lys34 and Glu134 in close proximity to each other likely creating one molecular surface forming a “hot spot” of biological activity. In Chapter IV I confirmed my low resolution structural data via peptide competition experiments where I identified peptides that can be used as scaffolds for future drug design. HIV-1 Vif oligomerization is concentration dependent. The HIV-1 Vif peptides Vif(29-43) and Vif(125-139) were able to disrupt HIV-1 Vif oligomerization, which confirms the low resolution structural data. HIV-1 Vif peptides Vif(25-39) and Vif(29-43) reduced the amount of APOBEC3G immobilized on the Protein A beads, reduced the amount of HIV-1 Vif interacting with APOBEC3G, or degraded APOBEC3G itself. These peptides could be used as scaffolds to design novel drugs that disrupt the function of HIV-1 Vif and or APOBEC3G. Therefore, low resolution structural data and peptide competition experiments were successful in identifying structurally important domains in HIV-1 Vif. They also provided insight into a possible mechanism for HIV-1 Vif function where a disorder-to-order transition facilitates HIV-1 Vif’s ability to interact with a diverse set of macromolecules. These data advance our structural understanding of HIV-1 Vif and they will facilitate future highresolution studies and novel drug designs.

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5

Tanaka, Masakazu. "Downregulation of CD4 is required for maintenance of viral infectivity of HIV-1". Kyoto University, 2003. http://hdl.handle.net/2433/148745.

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6

Rosa, Annachiara. "The cellular and molecular basis of the Nef requirement for HIV-1 infectivity". Doctoral thesis, Università degli studi di Trento, 2016. https://hdl.handle.net/11572/369203.

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Nef is an HIV -1 accessory protein with a fundamental role for virus replication in vivo and for the development of AIDS. Among its several activities, Nef is essential for full HIV-1 infectivity, a function highly prominent in lymphoid cells. So far, the mechanism by which Nef promotes HIV-1 infectivity has remained elusive. Over the course of 3 years, my PhD research activity has led to the identification of the host transmembrane protein SERINC5, and to a lesser extent SERINC3, as potent inhibitors of HIV-1 infectivity counteracted by the viral protein Nef [Rosa et al., 2015]. SERINC5 is predominantly localized on the plasma membrane where it is efficiently incorporated into budding HIV-1 virions and impairs subsequent virion penetration of susceptible target cells. Nef relocalizes SERINC5 to an endosomal compartment preventing its incorporation into HIV-1 particles. The ability to counteract SERINC5 is conserved in Nef proteins encoded by different primate immunodeficiency viruses, as well as in the structurally unrelated glycosylated Gag from murine leukaemia virus (MLV). These examples of functional conservation and convergent evolution emphasize the fundamental importance of SERINC5 in the interaction of the host with retroviral pathogens. Remarkably, SERINC5 potently inhibits HIV-1 even in the presence of Nef in a dose-dependent manner, suggesting that this cellular factor might be exploited as an anti-HIV-1 therapeutic gene.

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7

Krapp, Christian [Verfasser]. "Guanylate binding protein 5 is an interferon-inducible inhibitor of HIV-1 infectivity / Christian Krapp". Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1084767775/34.

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8

Meyer, Bahiah. "The role of HIV-1 subtype B Envelope transmission motifs in subtype C variant infectivity". Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29420.

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Transmitted founders (TF) might carry motifs that provide a phenotypic advantage that enables human immunodeficiency virus type-1 (HIV-1) to overcome immune barriers within the female genital tract. One study compared over 5000 subtype B TF and mismatched chronic infection envelope (env) sequences and identified two putative transmission motifs: Histidine at position 12 of the signal peptide (His12) and a potential N-glycan site (PNG) at position 413-415. Although, His12 was shown to be important for subtype B Env expression and viral infectivity, in our own sequence analysis subtype C variants did not carry the transmission motifs and the aim of this study was to determine whether His12 and PNG413 was important for subtype C Env expression, processing, function and viral replication. Mutagenesis of a subtype C Env clone indicated that His12 decreased pseudovirion (PSV) entry efficiency without influencing Env expression, secretion and cleavage with no changes in the N-glycosylation profile. This suggested that His12 had a fitness cost and was thus selected against. However, His12 significantly enhanced the entry efficiency of infectious molecular clones (IMCs), suggesting that it might be beneficial for in vivo replication. The variation between the PSV and IMC entry of TZM-bl cells could be due to differences in assay conditions. On the other hand deletion of PNG413 enhanced Env expression, secretion, cleavage and PSV and IMC entry efficiency of TZM-bl cells. This would suggest that subtype C TFs carrying a PNG at 413-413 would have lower viral replicative capacity due to poor expression and processing of Env. The benefit of this phenotype on HIV-1 subtype C transmission needs to be further investigated. Unfortunately, PSV and IMC entry of TZM-bl cells could not be confirmed by IMC replication in peripheral blood monocytes because the clones could not replicate to measurable levels in these cells over the culture period. Overall, this study has shown that amino acid residues at positions 12 and 415 do play a role in modulating Env processing and function however the actual mechanism by which these polymorphisms impact viral fitness most likely differ to that of subtype B, explaining why His12 is absent and PNG413 is present in subtype C TFs.

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9

Camaur, Diana M. "Roles of virion associated proteins in HIV-1 infectivity : Vif, Nef and the matrix tyrosine kinase /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9814538.

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10

Clemens, Rebecca [Verfasser]. "Characterization of a lipoprotein CD1348 from Clostridium difficile and the viral infectivity factor of HIV-1 / Rebecca Clemens". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2018. http://d-nb.info/1163804703/34.

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Capítulos de libros sobre el tema "HIV-1 infectivity"

1

Düzgüneş, Nejat, Charles E. Larsen, Krystyna Konopka, Dennis R. Alford, Lawrence J. T. Young, Thomas P. McGraw, Brian R. Davis, Shlomo Nir y Myra Jennings. "Fusion of HIV-1 and SIVmac with Liposomes and Modulation of HIV-1 Infectivity". En Mechanisms and Specificity of HIV Entry into Host Cells, 167–92. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5976-0_11.

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DeCamp, Dianne L., Lilia M. Babé, Paul Furth, Paul Ortiz de Montellano, Irwin D. Kuntz y Charles S. Craik. "Structure-Based Inhibition of HIV-1 Protease Activity and Viral Infectivity". En Advances in Experimental Medicine and Biology, 489–92. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6012-4_62.

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3

Johnson, Victoria A., Roy E. Byington y Peter L. Nara. "Quantitative Assays for Virus Infectivity". En Techniques in HIV Research, 71–86. London: Palgrave Macmillan UK, 1990. http://dx.doi.org/10.1007/978-1-349-11888-5_4.

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Di Bello, Carlo, Monica Dettin, Silvia Tormene y Rossella Roncon. "The structure of synthetic peptides from the principal neutralizing domain of HIV-1 gp120 affects binding to CD4 and viral infectivity". En Peptide Chemistry 1992, 437–38. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1474-5_129.

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Di Bello, Carlo, Monica Dettin, Silvia Tormene, Rossella Roncon, Andrea Bagno y Silvio Bicciato. "Conformational studies on synthetic peptides from the principal neutralizing domain of HIV-1 Gp120 that bind to CD4 and enhance viral infectivity". En Peptides, 95–97. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-010-9066-7_27.

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Hadeler, K. P. "Structured Population Models for HIV Infection Pair Formation and Non-constant Infectivity". En AIDS Epidemiology, 156–73. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4757-1229-2_8.

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Beck, Zoltan y Carl R. "Interactions of Infectious HIV-1 Virions with Erythrocytes: Implications for HIV-1 Pathogenesis and Infectivity". En HIV-Host Interactions. InTech, 2011. http://dx.doi.org/10.5772/24074.

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8

Caroline, Subra, Burelout Chantal, Proulx Sophie, Simard Sebastien y Gilbert Caroline. "Exosomes Decrease In Vitro Infectivity of HIV-1 Preparations: Implication for CD4+T Lymphocyte Depletion In Vivo". En Understanding HIV/AIDS Management and Care - Pandemic Approaches in the 21st Century. InTech, 2011. http://dx.doi.org/10.5772/19846.

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Taber, Douglass F. "The Boger Synthesis of (+)-Complestatin". En Organic Synthesis. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199965724.003.0102.

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(+)-Complestatin 3 shows promising activity against HIV infectivity. Dale L. Boger of Scripps/La Jolla described (J. Am. Chem. Soc. 2010, 132, 7776) an elegant multicomponent assembly of 3, the key step of which was the atropisomer-selective intramolecular Larock cyclization of 1 to 2. The preparation of 1 began with the protected phenethylamine 5, prepared by Sharpless asymmetric aminohydroxylation of the styrene 4. Conversion of 5 to the areneboronic acid followed by coupling with 6 delivered 7. Acylation led to 8, with the stage set for nitro-assisted addition-elimination, to form the first bis-aryl ether of 3. The product was a mixture of atropisomers, subsequently symmetrized to 9 by removal of the nitro group. Acylation of 9 led to 1. The role of the silyl group on the alkyne of 1 was to direct the regioselectivity of the intramolecular Larock indole synthesis. Again, two atropisomers were possible from the cyclization. Earlier model studies had suggested some preference for one over the other. As it turned out, in this case the desired atropisomer was the only one observed. It is particularly striking that the coupling was efficient even in the presence of the readily reduced and unprotected chlorophenols. The modular nature of this route to (+)-complestatin 3 will make it possible to prepare a variety of analogues. As long as only the substituents on the periphery are changed, the atropisomer selectivity in the Larock cyclization should be maintained.

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Actas de conferencias sobre el tema "HIV-1 infectivity"

1

Ke, Hengming, Yingdong Zhao, Yongquan Chen, Mike Schutkowski y Günter Fischer. "Is the cis-trans isomerization of cyclophilin involved in HIV-1 infectivity?" En Future Aspect in Peptide Chemistry - Ringberg Conference. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199901187.

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