Relevant bibliographies by topics / HIV Receptors

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'HIV Receptors'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "HIV Receptors"

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Shimizu, Nobuaki, Atsushi Tanaka, Atsushi Oue, Takahisa Mori, Chatchawann Apichartpiyakul, and Hiroo Hoshino. "A short amino acid sequence containing tyrosine in the N-terminal region of G protein-coupled receptors is critical for their potential use as co-receptors for human and simian immunodeficiency viruses." Journal of General Virology 89, no. 12 (December 1, 2008): 3126–36. http://dx.doi.org/10.1099/vir.0.2008/002188-0.

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Various G protein-coupled receptors (GPCRs) have the potential to work as co-receptors for human and simian immunodeficiency virus (HIV/SIV). HIV/SIV co-receptors have several tyrosines in their extracellular N-terminal region (NTR) as a common feature. However, the domain structure of the NTR that is critical for GPCRs to have co-receptor activity has not been identified. Comparative studies of different HIV/SIV co-receptors are an effective way to clarify the domain. These studies have been carried out only for the major co-receptors, CCR5 and CXCR4. A chemokine receptor, D6, has been shown to mediate infection of astrocytes with HIV-1. Recently, it was also found that an orphan GPCR, GPR1, and a formyl peptide receptor, FPRL1, work as potent HIV/SIV co-receptors in addition to CCR5 and CXCR4. To elucidate more about the domain of the NTR critical for HIV/SIV co-receptor activity, this study analysed the effects of mutations in the NTR on the co-receptor activity of D6, FPRL1 and GPR1 in addition to CCR5. The results identified a number of tyrosines that are indispensable for the activity of these co-receptors. The number and positions of those tyrosines varied among co-receptors and among HIV-1 strains. Moreover, it was found that a small domain of a few amino acids containing a tyrosine is critical for the co-receptor activity of GPR1. These findings will be useful in elucidating the mechanism that allows GPCRs to have the potential to act as HIV/SIV co-receptors.
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Garzino-Demo, Alfredo, and Robert C. Gallo. "HIV receptors on lymphocytes." Current Opinion in Hematology 10, no. 4 (July 2003): 279–83. http://dx.doi.org/10.1097/00062752-200307000-00005.

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Broder, Christopher C., and Ronald G. Collman. "Chemokine receptors and HIV." Journal of Leukocyte Biology 62, no. 1 (July 1997): 20–29. http://dx.doi.org/10.1002/jlb.62.1.20.

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Freeman, Tracey L., and Talia H. Swartz. "Purinergic Receptors: Elucidating the Role of these Immune Mediators in HIV-1 Fusion." Viruses 12, no. 3 (March 7, 2020): 290. http://dx.doi.org/10.3390/v12030290.

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Purinergic receptors are inflammatory mediators activated by extracellular nucleotides released by dying or injured cells. Several studies have described an important role for these receptors in HIV-1 entry, particularly regarding their activity on HIV-1 viral membrane fusion. Several reports identify purinergic receptor antagonists that inhibit HIV-1 membrane fusion; these drugs are suspected to act through antagonizing Env-chemokine receptor interactions. They also appear to abrogate activity of downstream mediators that potentiate activation of the NLRP3 inflammasome pathway. Here we review the literature on purinergic receptors, the drugs that inhibit their function, and the evidence implicating these receptors in HIV-1 entry.
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Jotwani, R., M. Muthukuru, and C. W. Cutler. "Increase in HIV Receptors/Co-receptors/α-defensins in Inflamed Human Gingiva." Journal of Dental Research 83, no. 5 (May 2004): 371–77. http://dx.doi.org/10.1177/154405910408300504.

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Transmission of HIV-1 through the oral cavity is considered to be a rare event. To identify factors in resistance/susceptibility to oral HIV-1 infection, we analyzed expression in human gingiva of HIV-1 receptors Langerin, DC-SIGN, MR, and GalCer, HIV-1 co-receptors CCCR5, CXCR4, and anti-microbial protein α-defensin-1. Our results show that healthy gingiva is infiltrated with cells expressing all HIV-1 receptors tested; however, there are very few CCR5+ cells and a complete absence of CXCR4+ cells in the lamina propria. In chronic periodontitis (CP), DC-SIGN, MR, CXCR4, and CCR5 increase, but this was accompanied by a ten-fold increase in α-defensin-1 mRNA. The CCR5+ cells were revealed to be T-cells, macrophages, and dermal dendritic cells. Moreover, epithelial expression of GalCer and CXCR4 together was not apical and showed no trend with underlying inflammation. Thus, low expression of HIV-1 co-receptors in health and high expression of α-defensin during CP may comprise endogenous factors that provide protection from oral HIV-1 infection.
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Turville, Stuart G., Jim Arthos, Kelli Mac Donald, Garry Lynch, Hassan Naif, Georgina Clark, Derek Hart, and Anthony L. Cunningham. "HIV gp120 receptors on human dendritic cells." Blood 98, no. 8 (October 15, 2001): 2482–88. http://dx.doi.org/10.1182/blood.v98.8.2482.

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Abstract Dendritic cells (DCs) are important targets for human immunodeficiency virus (HIV) because of their roles during transmission and also maintenance of immune competence. Furthermore, DCs are a key cell in the development of HIV vaccines. In both these settings the mechanism of binding of the HIV envelope protein gp120 to DCs is of importance. Recently a single C-type lectin receptor (CLR), DC-SIGN, has been reported to be the predominant receptor on monocyte-derived DCs (MDDCs) rather than CD4. In this study a novel biotinylated gp120 assay was used to determine whether CLR or CD4 were predominant receptors on MDDCs and ex vivo blood DCs. CLR bound more than 80% of gp120 on MDDCs, with residual binding attributable to CD4, reconfirming that CLRs were the major receptors for gp120 on MDDCs. However, in contrast to recent reports, gp120 binding to at least 3 CLRs was observed: DC-SIGN, mannose receptor, and unidentified trypsin resistant CLR(s). In marked contrast, freshly isolated and cultured CD11c+ve and CD11c−ve blood DCs only bound gp120 via CD4. In view of these marked differences between MDDCs and blood DCs, HIV capture by DCs and transfer mechanisms to T cells as well as potential antigenic processing pathways will need to be determined for each DC phenotype.
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Doepper, S., L. Kacani, B. Falkensammer, M. Dierich, and H. Stoiber. "Complement Receptors in HIV Infection." Current Molecular Medicine 2, no. 8 (December 1, 2002): 703–11. http://dx.doi.org/10.2174/1566524023361826.

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Doms, Robert W. "Fusing HIV and Chemokine Receptors." Journal of Immunology 186, no. 11 (May 19, 2011): 6073–75. http://dx.doi.org/10.4049/jimmunol.1100982.

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Weiss, Robin A. "HIV Receptors and Cellular Tropism." IUBMB Life (International Union of Biochemistry and Molecular Biology: Life) 53, no. 4-5 (April 1, 2002): 201–5. http://dx.doi.org/10.1080/15216540212652.

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Jiang, Shibo. "HIV-1 — co-receptors binding." Nature Medicine 3, no. 4 (April 1, 1997): 367–68. http://dx.doi.org/10.1038/nm0497-367.

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Dissertations / Theses on the topic "HIV Receptors"

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Shi, Yu. "Coreceptor usage and sensitivity to neutralization of HIV-1 and HIV-2 /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-093-1/.

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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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Bernhard, Oliver Karl. "Proteomic Investigation of the HIV Receptors CD4 and DC-Sign/CD209." University of Sydney. Medicine, 2004. http://hdl.handle.net/2123/585.

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HIV infection and disease is a multistage process that involves a variety of cell types as the virus spreads through the body. Initially, dendritic cells (DCs) present at the mucosal site of infection bind and internalise HIV for degradation and presentation to T cells. As the DCs migrate to lymph nodes and mature, part of the internalised virions remains infective inside endosomal compartments. During formation of the immunological synapse between CD4 T cells and DCs, infective virions from dendritic cells are transferred to CD4 T cells leading to a strong infection of those cells allowing rapid virus dissemination throughout the body and establishment of the typical HIV infection. Various membrane receptors are involved in this process. Initial HIV binding to DCs is mediated by C-type lectin receptors such as the mannose receptor or DC-SIGN (DC specific intracellular adhesion molecule 3 grabbing non integrin) which is followed by virus internalisation and lysis albeit virus induced changes in endocytic routing prevents a proportion from degradation. Productive infection of DCs has also been observed allowing trans infection of CD4 T cells through a different mechanism. HIV infection of CD4 T cells, DCs and other cells is a multistep process initiated by binding of HIV envelope gp120 to the CD4 receptor, a 55 kDa transmembrane glycoprotein. Subsequent conformational changes in gp120 allow binding to a chemokine receptor, either CCR5 or CXCR4, followed by membrane fusion and infection. The aim of this thesis was to investigate protein associations with the HIV receptors DC-SIGN and CD4 in order to elucidate the mechanism of complex formation, virus entry and/or defining target sites for antiretroviral drugs. This thesis used a proteomic approach for studying the receptors with mass spectrometry-based protein identification as its core technology. A range of different approaches were developed and compared for identification of protein interactions and characterisation of the identified protein associations. An affinity purification of the CD4 receptor complex from lymphoid cells was used as the basis for detecting novel CD4-binding proteins. For this approach a strategy based on mass spectrometry identification of CD4 associating proteins using affinity chromatography and affinity-tag mediated purification of tryptic peptides was developed. This method proved successful for the identification of CD4 interacting proteins such as the strongly associated kinase p56lck, however a limited number of non-specifically bound proteins were also identified along the receptor complex. Using one-dimensional SDS-polyacrylamide gel electrophoresis followed by in-gel digests and mass spectrometry analysis, a large number of non-specifically binding proteins were identified along the CD4/lck complex. Evaluation of different lysis buffers in several independent experiments demonstrated that there was a large and inconsistent array of proteins that were obviously non-specifically bound to the receptor. No further specific binding partners were detected. These data suggested that protein interactions of CD4 on this cell type are of weak and/or transient nature. It also demonstrated a need for careful interpretation of proteomic data in the light of the propensity of non-specific binding under these conditions. To overcome dissociation of weak protein interactions, a method was developed using chemical cross-linking to preserve weak protein interactions on lymphoid cells. Affinity purification was used to purify CD4 along with cross-linked associated proteins and mass spectrometry analysis identified an interaction with the transferrin receptor CD71 and the tyrosine phosphatase CD45. The CD45-CD4 interaction is well known. The CD4-CD71 interaction was demonstrated to be a result from colocalization of the two molecules during formation of endocytic vesicles. Flow cytometry-based fluorescence resonance energy transfer (FRET) measurements were applied to confirm colocalization. A similar interaction was suspected for CD4 and DC-SIGN on the plasma membrane of DCs as cis infection of DCs has been demonstrated i.e. initial binding to DC-SIGN then to CD4/CCR5 on the same cell. Therefore, protein associations of DC-SIGN were investigated using the developed techniques. Using cross-linking, DC-SIGN was shown to assemble in large complexes on the surface of immature monocyte-derived DCs. Mass spectrometry analysis of the purified complexes identified them as homo-oligomers of DC-SIGN. The absence of CD4 suggested that the fraction interacting with CD4 at any one time must be small. The complexes of DC-SIGN were further characterised to be tetramers and successfully co-immunoprecipitated with HIV gp120 and mannan. DC-SIGN monomers were not evident demonstrating that the assembly of DC-SIGN into tetramers is required for high affinity binding of its natural and viral ligands. Thus potential antiviral agents aimed at blocking the early stage of HIV binding to DCs must simulate tetramers in order to neutralise the virus efficiently. Overall the thesis provides new information on protein interactions of CD4 and DC-SIGN, a careful investigation of "proteomics" techniques for identifying the proteins in affinity-purified samples and demonstrates the need for multifaceted analytical approaches to probe complex cellular systems.
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Boulet, Salix. "Natural Killer cell receptors and decreased susceptibility to HIV infection." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86647.

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The human immunodeficiency virus (HIV) currently infects over 33 million individuals worldwide. The development of a protective HIV vaccine would provide the ideal tool to fight this pandemic. Recent clinical trials testing candidate T- and B-cell based vaccine strategies have failed to demonstrate that these were protective against infection. For many, these failures underline how little is known about what constitutes an efficient immune response against HIV and that increased knowledge about the role of innate immune cells may be required in order to design an efficient vaccine against HIV.
Natural Killer (NK) cells are part of the innate arm of the immune system and are involved in the control of several viral infections, including HIV. Epidemiological evidence has linked specific NK cell receptors, termed KIR3DS1 and KIR3DL1, to favourable clinical outcomes in HIV infected individuals. Whether these receptors would also be involved in protection from infection, and therefore could provide the basis for new vaccine strategies, is unknown.
To address this question, we have evaluated the genetic distribution of both KIR3DS1 and KIR3DL1 in a population of exposed uninfected individuals (EUs). EUs remain HIV seronegative despite repeated exposure to the virus through high-risk behavior. Understanding the immunological causes of their decreased susceptibility to infection may provide insights into vaccine design. In chapter II we demonstrate that KIR3DS1 homozygous individuals are overrepresented in the EU population. Additionnally, in chapter III, we provide evidence that the combined genotype of HLA-B*57 with a specific set of KIR3DL1 alleles is also overrepresented in the EU population. Finally, in chapter IV, we demonstrate that NK cells from individuals carrying certain KIR3DL1/HLA genotypes linked to slower HIV disease progression and/or protection from infection have increased functional potential following stimulation.
The evidence presented in this thesis supports a role for NK cells, and particularly of KIR3DS1 and KIR3DL1, in the decreased susceptibility to HIV infection observed in EUs. Given that these cells are directly involved in viral suppression and are capable of modulating both the adaptive and innate arm of the immune response, understanding how NK cell mediate these activities may reveal new therapeutic strategies against HIV.
Le virus de l'immunodéficience humaine (VIH) infecte présentement plus de 33 millions d'individus. Contre cette pandémie, la solution idéale serait le développement d'un vaccin. Toutefois, de récents essais cliniques évaluant l'efficacité des stratégies de vaccination visant à la stimulation des cellules T ou B contre le VIH n'ont pas réussi à démontrer que ces stratégies protégeaient contre l'infection. Pour plusieurs membres de la communauté scientifique, ces échecs démontrent que les caractéristiques d'une réponse immunitaire efficace contre le VIH sont encore méconnues et que le rôle des cellules du système immun inné devra sans doute être éclairci afin d'élaborer un vaccin efficace contre le VIH.
Les cellules NK (Natural Killer) font parties du système immunitaire inné et aident au contrôle de plusieurs infections virales, incluant les infections au VIH. Des études épidémiologiques ont lié certains récepteurs des cellules NK, appelés KIR3DS1 et KIR3DL1, à des indices cliniques favorables chez des individus infectés par le VIH. Que ces récepteurs puissent aussi pourvoir une forme de protection contre l'infection, et donc inspirer de nouvelles stratégies de vaccination, demeure encore incertain.
Afin de répondre à cette question, nous avons évalué la distribution génétique de KIR3DS1 et KIR3DL1 dans une population d'individus exposés séronégatifs (ESN). Les ESN demeurent séronégatifs aux anticorps du VIH malgré des comportements à risques. Comprendre les facteurs immunitaires permettant à cette population d'être moins susceptible à l'infection au VIH pourrait aider à l'élaboration d'un vaccin. Lors du chapitre II, nous démontrons que les individus KIR3DS1 homozygotes sont surreprésentés dans la population d'ESN. De plus, dans le troisième chapitre, nos données soutiennent qu'une combinaison génétique du HLA-B*57 avec un sous-type particulier de KIR3DL1 et aussi surreprésentée dans la population d'ESN. Finalement, dans le chapitre IV, nous démontrons que les cellules NK provenant d'individus ayant des génotypes HLA/KIR3DL1 liés à une progression plus lente de la maladie VIH et/ou à une protection contre l'infection ont un potentiel de fonctionnalité accru suivant une stimulation.
Les données présentées dans cette thèse suggèrent que les cellules NK, plus particulièrement leurs récepteurs KIR3DS1 et KIR3DL1, sont impliquées dans une forme de résistance à l'infection observée chez les ESN. Puisque ces cellules sont directement impliquées dans le contrôle viral et peuvent moduler à la fois le système immun inné et adapté, éclaircir les mécanismes permettant aux cellules NK de diminuer la susceptibilité à l'infection pourrait révéler de nouvelle stratégie thérapeutique afin de contrer le VIH.
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Clevestig, Peter. "HIV-1 phenotype and genetic variation in vertical transmission /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-631-X/.

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Jacobs, Caron Adrienne. "The nanoscale organisation of HIV cell surface receptors CD4 and CCR5." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10056281/.

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The plasma membrane serves as the cell’s front line for interactions with, and response to, the external environment. The molecular mechanisms and regulation of cellular responses to extracellular signals are determined by the spatial organisation and dynamics of the various components comprising the plasma membrane. CD4 and CCR5 are two key cell surface molecules with important roles in immune cell function and regulation. They are also co-opted as the primary receptor and a co-receptor, respectively, by HIV. Biochemical studies have provided a detailed understanding of the molecular mechanisms of these interactions. Until recently, however, the small scale and rapid dynamics of these interactions has meant that a detailed view of the topology of the cell membrane and the organisation of receptors first encountered by the virus has been beyond the resolving power of available tools. The increasing capabilities of the emerging and rapidly developing super-resolution microscopy technologies are now optimally poised for us to address some of these questions. In this work, I have applied single molecule localization microscopy to unveil some of the nanoscale organisational properties of the cell surface receptors CD4 and CCR5. I have worked on the development of small labelling probes for CD4 and addressed some of the key aspects of sample preparation and labelling that can artificially alter the distribution of membrane associated target molecules. Here I report the first quantitative characterisation of the nanoscale organisation of CD4 and CCR5 in lymphoid cell plasma membranes, as well as how this organisation changes under different conditions, such as in response to cell signal-mimicking stimulation, or exposure to HIV envelope. This approach to characterising membrane receptor organisation can be further applied to in-depth studies of early host cell-virus interactions, as well as to other cell surface receptors and their organisation in the context of key cellular functions.
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Sorrell, Mary. "The Role of P2X Receptors in HIV and Opiate-Related Neurotoxicity." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3405.

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Emerging evidence suggests that opioid drugs can exacerbate neuroAIDS. Microglia are the principal neuroimmune effectors thought to be responsible for neuron damage in HIV-infected individuals, and evidence suggests that drugs acting via opioid receptors in microglia aggravate the neuropathophysiological effects of HIV. The P2X family of ATP activated ligand-gated ion channels regulates key aspects of microglial function. In addition, opioid-dependent microglial activation has been reported to be mediated through P2X4 signaling, prompting us to investigate P2X receptors contribution to the neurotoxic effects of HIV and morphine. In vitro experiments showed treatment with TNP-ATP prevented the neurotoxic effects of morphine and/or HIV Tat, or ATP alone in a concentration dependent manner. This evidence suggests P2X receptors mediate the neurotoxic effects of these insults in striatal neurons. P2X1, P2X3, and P2X7 selective receptor antagonists did not prevent Tat- and/or morphine-induced neurotoxicity, implying cellular pathways activated may not involve these subtypes. Cells from P2X4KO mice show that activation of the P2X4 receptor on glia are necessary to cause Tat and/or morphine toxicity. However, data implied that baseline neuronal function may be altered due to lack of P2X4 receptor expression, and also gave evidence for altered Tat and morphine cellular signaling when the two are given in combination versus alone. Surgeries were performed on P2X4 KO and WT mice, which received intrastriatal Tat injections and morphine and/or naltrexone pellets. WT mice showed significant increases in inflammatory markers when treated with Tat and/or morphine. Increases in inflammatory markers were not seen in P2X4 KO mice, implying P2X4 receptors play a role in neuroinflammation resulting from Tat and/or morphine. Finally, human tissue samples from the National NeuroAIDS Tissue Consortium were analyzed. Changes in P2X5 and P2X7 mRNA were found in microarray data, but only changes in P2X7 mRNA levels were confirmed by RT-PCR. No changes in P2X4 mRNA levels were detected. Our experiments indicate the P2X receptor family contributes to Tat- and morphine- related neuronal injury, and reveal that members of the P2X receptor family, especially P2X4, may be novel therapeutic targets for restricting the synaptodendritic injury and neurodegeneration that accompany neuroAIDS and opiate abuse.
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Moore, David Joseph. "Regional neuropathology and cognitive abilities in HIV infection /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3083453.

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Valiathan, Rajeshwari Rajan. "Functional interactions of HIV-1 GAg with the cellular endocytic pathway /." Access full-text from WCMC, 2007. http://proquest.umi.com/pqdweb?did=1481666381&sid=16&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Berbaum, Jennifer Bentz Joe. "Investigating the role of nuclear receptors in HIV/HAART-associated dyslipidemic lipodystrophy /." Philadelphia, Pa. : Drexel University, 2007. http://hdl.handle.net/1860/1759.

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Books on the topic "HIV Receptors"

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Dimitrov, Dimiter S. HIV and membrane receptors. New York: Chapman & Hall, 1997.

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Meucci, Olimpia. Chemokine receptors and neuroAIDS: Beyond co-receptor function and links to other neuropathologies. New York: Springer, 2010.

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O, Freed Eric, and SpringerLink (Online service), eds. HIV Interactions with Host Cell Proteins. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Clavel, François. HIV: Portrait of a complex retrovirus, [and], A second receptor for AIDS virus? Sudbury, Ont: Laurentian University, School of Translators and Interpreters, 1996.

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Dimitrov, Dimiter S. HIV Receptors And Membrane Receptors. Landes Bioscience, 2005.

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Dimitrov, Dimiter S. HIV And Membrance Receptors. 2nd ed. Landes Bioscience, 2006.

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(Editor), D. S. Dimitrov, and C. C. Broder (Editor), eds. Hiv and Membrane Receptors (Medical Intelligence Unit). Springer Verlag, 1997.

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1950-, O'Brien Thomas, ed. Chemokine receptors and AIDS. New York: Marcel Dekker, 2002.

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B, Kendow Lawrence, ed. AIDS vaccines, HIV receptors, and AIDS research. New York: Nova Science Publishers, 2008.

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Meucci, Olimpia. Chemokine Receptors and NeuroAIDS. Springer, 2010.

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Book chapters on the topic "HIV Receptors"

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Tan, Kevin, Avindra Nath, and Ahmet Hoke. "HIV Infection and the PNS." In Chemokine Receptors and NeuroAIDS, 51–85. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_4.

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Chen, Maria F., Samantha Soldan, and Dennis L. Kolson. "HIV Neuroinvasion: Early Events, Late Manifestations." In Chemokine Receptors and NeuroAIDS, 5–31. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_2.

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Fischer-Smith, Tracy, and Jay Rappaport. "HIV Co-receptors: The Brain Perspective." In Chemokine Receptors and NeuroAIDS, 33–50. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_3.

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Banerjee, Anupam, Michael R. Nonnemacher, and Brian Wigdahl. "HIV Latency and Reactivation: Role in Neuropathogenesis." In Chemokine Receptors and NeuroAIDS, 87–118. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_5.

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Vergote, David, Christopher M. Overall, and Christopher Power. "Chemokine Proteolytic Processing in HIV Infection: Neurotoxic and Neuroimmune Consequences." In Chemokine Receptors and NeuroAIDS, 149–72. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_7.

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Klein, Robyn S., and Erin E. McCandless. "HIV Coreceptors and Their Roles in Leukocyte Trafficking During Neuroinflammatory Diseases." In Chemokine Receptors and NeuroAIDS, 119–46. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_6.

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Hauser, Kurt F., Nazira El-Hage, Annadora J. Bruce-Keller, and Pamela E. Knapp. "Opioids, Astroglial Chemokines, Microglial Reactivity, and Neuronal Injury in HIV-1 Encephalitis." In Chemokine Receptors and NeuroAIDS, 353–77. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_16.

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Murphy, Philip M. "Roles for Chemokine Receptors in HIV Pathogenesis." In National Institute of Allergy and Infectious Diseases, NIH, 53–57. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-512-5_6.

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Happel, Christine, Changcheng Song, Mathew J. Finley, and Thomas J. Rogers. "Interaction Between Opioid and Chemokine Receptors in Immune Cells: Implications for HIV Infection." In Chemokine Receptors and NeuroAIDS, 319–35. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_14.

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Montefiori, David C. "Role of complement and Fc receptors in the pathogenesis of HIV-1 infection." In Immunopathogenesis of HIV Infection, 119–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60867-4_9.

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Conference papers on the topic "HIV Receptors"

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Hansi, R., G. K. Singhera, T. Guo, C. Leung, T. Shaipanich, D. D. Sin, D. R. Dorscheid, and J. M. Leung. "Interactions Between HIV and the Airway: HIV Receptor and Co-Receptor Expression in the Airway Epithelium." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2683.

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Fogel, Gary B., Enoch S. Liu, Marco Salemi, Susanna L. Lamers, and Michael S. McGrath. "Evolved neural networks for HIV-1 co-receptor identification." In 2014 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2014. http://dx.doi.org/10.1109/cec.2014.6900628.

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Zhang, Xiao-Yi, Cun Xin Wang, and Kun Zeng. "Two Receptor Based Pharmacophore Models for HIV-1 Integrase DKA Inhibitors." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2009). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163720.

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Charon, M. H., L. Tranqui, A. Andrieux, G. Hudry-Clergeon, and G. Marguerie. "FIBRINOGEN BINDING TO ENDOTHELIAL CELLS AND INTERFERING PEPTIDES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644735.

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Fibrinogen interacts with platelets and endothelial cells via specific binding sites. While the platelet fibrinogen receptor has been identified and was found to be associated with GPIIb-IIIa, the binding site on endothelial cells has not been characterized yet. The platelet GPIIb-IIIa belongs to the newly identified cytoadhesin family which includes immunologicaly related receptors interacting with RGD containing proteins. A cytoadhesin has recently been described on endothelial cells and the possibility that fibrinogen might interact with this glycoprotein was examined. Peptides corresponding to γ and α chains sequences were synthesized and their capacity to inhibit fibrinogen binding to endothelial cells and platelets were compared. Analogues of the γ chain from His 400 to Val 411 produced an inhibition similar to that observed for fibrinogen platelet interaction, suggesting that the structure function relationship of γ peptides is identical in both systems. In contrast synthetic analogues corresponding to the a chain and including RGD yielded slightly different results. While RGD alone was inactive on platelet, this tripeptide was active on endothelial cells. RGDS and RGDF corresponding to α 572-575 and α 95-98 partially or fully inhibited fibrinogen binding to endothelial cells but the structure activity relationship was different when compared to that observed for platelets. Addition of the N and C sequences adjacent to RGDS reduced the activity of this peptide whereas the activity of RGDF analogues was not modified by addition of N and C-sequences. In contrast platelet fibrinogen binding decreased with these RGDF analogues. These results suggest that fibrinogen endothelial cell binding is mediated by an RGD adhesion receptor with subtle differences in the recognition selectivity of the ligand, which is controled by the surrounding sequence.
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Dhillon, Navneet K., Pranjali Dalvi, and Amy O'Brien-Ladner. "HIV-Tat And Cocaine Mediated Down-Regulation Of BMP Receptor Axis In Pulmonary Smooth Muscle Cells: Implications For HIV-PAH." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2615.

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Latham, Heath E., Amy O'Brien-Ladner, Pranjali Dalvi, Yuqiao Dai, and Navneet K. Dhillon. "Cigarette Smoke Condensate Down-Regulates Interferon-Gamma Receptor In HIV-Infected Human Macrophages." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6053.

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Moroi, M., S. M. Jung, N. Yoshida, N. Aoki, and K. Tanoue. "THROMBASTHENIA WITH AN ABNORMAL PLATELET MEMBRANE GPIIb OF DIFFERENT MOLECULAR WEIGHT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644741.

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We describe several individuals with abnormal platelet glycoprotein lib (GPIIb) of different molecular weight (MW), a novel defect in that previously reported thrombasthenics have not shown GPIIb molecules of abnormal MW. Patient 1 shows 2 bands of GPIIb (one with normal MW and one with abnormal MW) in SDS-PAGE (lectin and antibody staining). This patient has a mild bleeding tendency, and her platelets did not aggregate in response to ADP (2-10 μM) and had severely depressed collagen induced aggregation ,but responded normally to ristocetin. The MW of the abnormal GPIIb band was calculated to be 122 KDa (compared to the 129 kDa of normal GPIIb) in non-reduced SDS-PAGE; the MW was 128 kDa (compared to the normal 118 kDa) in reduced SDS-PAGE. The amount of each GPIIb band, calculated from densitometry, was approximately 35% for the GPIIb of abnormal MW and 20% for the normal MW GPIIb, relative to the amounts of GPIIb found in normal individuals. Assays of fibrinogen binding to the patient`s platelets indicate that they contain 25% of the fibrinogen receptor as compared to normal platelets. Crossed immunoelectrophoresis showed the formation of the GPIIb/IIIa complex, which was found to consist mostly of normal MW GPIIb and GPIIIa. The patient's father showed decreased aggregability in response to ADP, and his platelets also contained abnormal and normal GPIIb. The father's platelets, however, contained about 50% normal GPIIb as compared to normal platelets, and his platelets have about 50% the number of fibrinogen receptors compared to normal platelets. From these results, the patient was suggested to have heterozygous GPIIb molecules, and the observed defects in aggregability would be attributable to the decrease of normal GPIIb to 20-30% of the normal level. Quite recently, we found another thrombasthenic individual who has homozygous abnormal GPIIb molecules. Electrophoretic mobilities of his abnormal GPIIb on SDS-PAGE indicated that the abnormal GPIIb's were very similar between the 2 cases, and two-dimensional, unreduced-reduced SDS-PAGE suggested that the abnormal GPIIb consists of a single chain.
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Bezerra, Sarah Albuquerque, Raffaela Neves Mont'alverne Napoleão, Thaís Fontenelle Studart, Ana Beatriz Gomes Santiago, and José Carlos Araújo Fontenele. "PRINCIPAIS MECANISMOS IMUNOLÓGICOS DECORRENTES DA INFECÇÃO PELO VÍRUS DA IMUNODEFICIÊNCIA HUMANA (HIV): UMA REVISÃO DE LITERATURA." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/989.

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Introdução: O vírus da imunodeficiência humana (HIV) em sua forma aguda pode causar febre, cefaleia, mal-estar, astenia, diarreia, dermatite, faringite, sudorese noturna, entre outros sintomas. O HIV infecta aproximadamente 37 milhões de pessoas no aspecto global e mata cerca de 1 milhão de indivíduos por ano, o que o torna de grande importância. Uma das razões dos altos índices de morbimortalidade é a ausência de tratamentos efetivos. Nos últimos anos houveram muitos avanços farmacológicos, todavia, ainda não há cura para a patologia, apenas o controle por terapias antivirais. Desta forma, o conhecimento acerca da resposta imunológica do vírus e do seu destino intracelular torna-se crucial, assim como a atividade imune inata e as possíveis restrições do vírus HIV-1 por alguns genes. Objetivos: Descrever as principais alterações do sistema imunológico decorrentes da infecção por HIV. Material e método: Revisão de literatura que abrangeu 3 artigos científicos entre os anos de 2011-2021, em língua inglesa e portuguesa, tratando-se da infecção por HIV e suas implicações imunológicas nas seguintes bases de dados: PubMed, ScieLO e LILACS. As palavras-chave utilizadas foram "HIV","Imunodeficiências", "Imunologia". Resultados: As infecções por HIV podem ser ocasionadas por um ou mais retrovírus, HIV-1 e HIV-2. Esses retrovírus atravessam as mucosas do organismo, infectando células do sistema imune, especialmente os linfócitos CD4 +, os quais são destruídos por esse vírus de forma progressiva. Os linfócitos possuem receptores para o HIV, de tal forma que eles se ligam na membrana dessa célula e penetram no seu interior para se multiplicarem, o que, posteriormente, a partir dessa população de células infectadas, poderão ser disseminados para os linfonodos, que permitirão que o vírus se espalhe em número satisfatório para instituir e manter a produção de vírus nos tecidos linfoides, além de estabelecer um reservatório viral latente, principalmente em linfócitos CD4+. Conclusão: Destaca-se, portanto, que os indivíduos com HIV, devido à destruição dos seus linfócitos CD4+ e, consequentemente, o comprometimento do seu sistema imunológico, ficam suscetíveis ao ataque de organismos infecciosos, aumentando sua imunodeficiência que, em última análise, leva a doenças oportunistas características da AIDS.
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Geißler, C., Y. Foerster, M. Diensthuber, J. Wagenblast, S. Balster, J. Gabrielpillai, H. Petzold, and T. Stöver. "Neurotrophin receptors- prognostic markers and therapeutic targets for HNSCC?" In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727956.

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Mermis, Joel, Amy O'Brien-Ladner, and Navneet Dhillon. "HIV-Tat Potentiates The Proliferation Of Vascular Smooth Muscle Cells Through Induction Of PDGF/ PDGF- Receptor Axis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1176.

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Reports on the topic "HIV Receptors"

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Porter, Dale A., and Kornelia Polyak. Identification of a Receptor for Tumor Suppressor HIN-1. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416631.

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