Relevant bibliographies by topics / Protein-HIV Virus

Academic literature on the topic 'Protein-HIV Virus'

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Published: 6 September 2023

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Journal articles on the topic "Protein-HIV Virus"

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Travis, J. "HIV Protein Prepares Virus' Next Victims." Science News 152, no. 4 (July 26, 1997): 53. http://dx.doi.org/10.2307/3981058.

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Romani, Bizhan, and Susan Engelbrecht. "Human immunodeficiency virus type 1 Vpr: functions and molecular interactions." Journal of General Virology 90, no. 8 (August 1, 2009): 1795–805. http://dx.doi.org/10.1099/vir.0.011726-0.

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Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is an accessory protein that interacts with a number of cellular and viral proteins. The functions of many of these interactions in the pathogenesis of HIV-1 have been identified. Deletion of the vpr gene reduces the virulence of HIV-1 dramatically, indicating the importance of this protein for the virus. This review describes the current findings on several established functions of HIV-1 Vpr and some possible roles proposed for this protein. Because Vpr exploits cellular proteins and pathways to influence the biology of HIV-1, understanding the functions of Vpr usually involves the study of cellular pathways. Several functions of Vpr are attributed to the virion-incorporated protein, but some of them are attributed to the expression of Vpr in HIV-1-infected cells. The structure of Vpr may be key to understanding the variety of its interactions. Due to the critical role of Vpr in HIV-1 pathogenicity, study of the interactions between Vpr and cellular proteins may help us to understand the mechanism(s) of HIV-1 pathogenicity.
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Álvarez, Enrique, Alfredo Castelló, Luis Menéndez-Arias, and Luis Carrasco. "HIV protease cleaves poly(A)-binding protein." Biochemical Journal 396, no. 2 (May 15, 2006): 219–26. http://dx.doi.org/10.1042/bj20060108.

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The PABP [poly(A)-binding protein] is able to interact with the 3′ poly(A) tail of eukaryotic mRNA, promoting its translation. Cleavage of PABP by viral proteases encoded by several picornaviruses and caliciviruses plays a role in the abrogation of cellular protein synthesis. We report that infection of MT-2 cells with HIV-1 leads to efficient proteolysis of PABP. Analysis of PABP integrity was carried out in BHK-21 (baby-hamster kidney) and COS-7 cells upon individual expression of the protease from several members of the Retroviridae family, e.g. MoMLV (Moloney murine leukaemia virus), MMTV (mouse mammary tumour virus), HTLV-I (human T-cell leukaemia virus type I), SIV (simian immunodeficiency virus), HIV-1 and HIV-2. Moreover, protease activity against PABP was tested in a HeLa-cell-free system. Only MMTV, HIV-1 and HIV-2 proteases were able to cleave PABP in the absence of other viral proteins. Purified HIV-1 and HIV-2 proteases cleave PABP1 directly at positions 237 and 477, separating the two first RNA-recognition motifs from the C-terminal domain of PABP. An additional cleavage site located at position 410 was detected for HIV-2 protease. These findings indicate that some retroviruses may share with picornaviruses and caliciviruses the capacity to proteolyse PABP.
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Liu, Hongmei, Xiaoyun Wu, Hongling Xiao, and John C. Kappes. "Targeting Human Immunodeficiency Virus (HIV) Type 2 Integrase Protein into HIV Type 1." Journal of Virology 73, no. 10 (October 1, 1999): 8831–36. http://dx.doi.org/10.1128/jvi.73.10.8831-8836.1999.

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ABSTRACT Integrase (IN) is the only retroviral enzyme necessary for the integration of retroviral cDNA into the host cell’s chromosomes. The structure and function of IN is highly conserved. The human immunodeficiency virus type 2 (HIV-2) IN has been shown to efficiently support 3′ processing and strand transfer of HIV-1 DNA substrate in vitro. To determine whether HIV-2 IN protein (IN2) could substitute for HIV-1 IN function in vivo, we used HIV-1 Vpr to deliver the IN2 into IN mutant HIV-1 virions by expression intrans as a Vpr-IN fusion protein.Trans-complementation with IN2 markedly increased the infectivity of IN-minus HIV-1. Compared with the homologous trans-IN protein, infectivity was increased to a level of 16%. Since IN has been found to play a role in reverse transcription (Wu et al., J. Virol. 73:2126–2135, 1999), cells infected with IN2-complemented HIV-1 were analyzed for DNA products of reverse transcription. DNA levels of approximately 18% of that of wild type were detected. The homologous trans-IN protein restored the synthesis of viral cDNA to approximately 86% of that of wild-type virus. By complementing integration-defective HIV-1 IN mutant viruses, which were not impaired in cDNA synthesis, thetrans-IN2 protein was shown to support integration up to a level of 55% compared with that of the homologoustrans-IN protein. The delivery of heterologous IN protein into HIV-1 particles in trans offers a novel approach to understand IN protein function in vivo.
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Elalouf, Amir. "In-silico Structural Modeling of Human Immunodeficiency Virus Proteins." Biomedical Engineering and Computational Biology 14 (January 2023): 117959722311544. http://dx.doi.org/10.1177/11795972231154402.

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Human immunodeficiency virus (HIV) is an infectious virus that depletes the CD4+ T lymphocytes of the immune system and causes a chronic life-treating disease—acquired immunodeficiency syndrome (AIDS). The HIV genome encodes different structural and accessory proteins involved in viral entry and life cycle. Determining the 3D structure of HIV proteins is essential for new target position finding, structure-based drug designing, and future planning for computational and laboratory experimentations. Hence, the study aims to predict the 3D structures of all the HIV structural and accessory proteins using computational homology modeling to understand better the structural basis of HIV proteins interacting with host cells and viral replication. The sequences of HIV capsid, matrix, nucleocapsid, p6, reverse transcriptase, invertase, protease, gp120, gp41, virus protein r, viral infectivity factor, virus protein unique, RNA splicing regulator, transactivator protein, negative regulating factor, and virus protein x proteins were retrieved from UniProt. The primary and secondary structures of HIV proteins were predicted by Expasy ProtParam and SOPMA web servers. For the homology modeling, the MODELLER predicted the 3D structures of HIV proteins using templates. Then, the modeled structures were validated by the Ramachandran plot, local and global quality estimation scores, QMEAN scores, and Z-scores. Most of the amino acid residues of HIV proteins were present in the most favored and generously allowed regions in the Ramachandran plots. The local and global quality scores and Z-scores of the HIV proteins confirmed the good quality of modeled structures. The 3D modeled structures of HIV proteins might help further investigate the possible treatment.
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Coghlan, Andy. "Virus-sabotaging protein may help people defy HIV." New Scientist 220, no. 2940 (October 2013): 19. http://dx.doi.org/10.1016/s0262-4079(13)62520-8.

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Tang, Yao, Ulrike Winkler, Eric O. Freed, Ted A. Torrey, Wankee Kim, Henry Li, Stephen P. Goff, and Herbert C. Morse. "Cellular Motor Protein KIF-4 Associates with Retroviral Gag." Journal of Virology 73, no. 12 (December 1, 1999): 10508–13. http://dx.doi.org/10.1128/jvi.73.12.10508-10513.1999.

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ABSTRACT Previously we demonstrated that murine retroviral Gag proteins associate with a cellular motor protein, KIF-4. Using the yeast two-hybrid assay, we also found an association of KIF-4 with Gag proteins of Mason-Pfizer monkey virus (MPMV), simian immunodeficiency virus (SIV), and human immunodeficiency virus type 1 (HIV-1). Studies performed with mammalian cell systems confirmed that the HIV-1 Gag protein associates with KIF-4. Soluble cytoplasmic proteins from cells infected with recombinant vaccinia virus expressing the entire Gag-Pol precursor protein of HIV-1 or transfected with HIV-1 molecular clone pNL4-3 were fractionated by sucrose gradient centrifugation and further separated by size-exclusion and anion-exchange chromatographies. KIF-4 and HIV-1 Gag cofractionated in both chromatographic separations. Immunoprecipitation assays have also verified the KIF-4–Gag association. KIF-4 binds mainly to the Gag precursor (Pr55 Gag) and a matrix-capsid processing intermediate (Pr42) but not to other processed Gag products. The binding of Gag is mediated by a domain of KIF-4 proximal to the C terminus. These results, and our previous studies, raise the possibility that KIF-4 may play an important role in retrovirus Gag protein transport.
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Noble, Beth, Paolo Abada, Juan Nunez-Iglesias, and Paula M. Cannon. "Recruitment of the Adaptor Protein 2 Complex by the Human Immunodeficiency Virus Type 2 Envelope Protein Is Necessary for High Levels of Virus Release." Journal of Virology 80, no. 6 (March 15, 2006): 2924–32. http://dx.doi.org/10.1128/jvi.80.6.2924-2932.2006.

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ABSTRACT The envelope (Env) protein of human immunodeficiency virus type 2 (HIV-2) and the HIV-1 Vpu protein stimulate the release of retroviral particles from human cells that restrict virus production, an activity that we call the enhancement of virus release (EVR). We have previously shown that two separate domains in the HIV-2 envelope protein are required for this activity: a glycine-tyrosine-x-x-hydrophobic (GYxxθ) motif in the cytoplasmic tail and an unmapped region in the ectodomain of the protein. We here report that the cellular partner of the GYxxθ motif is the adaptor protein complex AP-2. The mutation of this motif or the depletion of AP-2 by RNA interference abrogated EVR activity and changed the cellular distribution of the Env from a predominantly punctate pattern to a more diffuse distribution. Since the L domain of equine infectious anemia virus (EIAV) contains a Yxxθ motif that interacts with AP-2, we used both wild-type and L domain-defective particles of HIV-1 and EIAV to examine whether the HIV-2 Env EVR function was analogous to L domain activity. We observed that the production of all particles was stimulated by HIV-2 Env or Vpu, suggesting that the L domain and EVR activities play independent roles in the release of retroviruses. Interestingly, we found that the cytoplasmic tail of the murine leukemia virus (MLV) Env could functionally substitute for the HIV-2 Env tail, but it did so in a manner that did not require a Yxxθ motif or AP-2. The cellular distribution of the chimeric HIV-2/MLV Env was significantly less punctate than the wild-type Env, although confocal analysis revealed an overlap in the steady-state locations of the two proteins. Taken together, these data suggest that the essential GYxxθ motif in the HIV-2 Env tail recruits AP-2 in order to direct Env to a cellular pathway or location that is necessary for its ability to enhance virus release but that an alternate mechanism provided by the MLV Env tail can functionally substitute.
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Fackler, Oliver T., Paola d'Aloja, Andreas S. Baur, Maurizio Federico, and B. Matija Peterlin. "Nef from Human Immunodeficiency Virus Type 1F12 Inhibits Viral Production and Infectivity." Journal of Virology 75, no. 14 (July 15, 2001): 6601–8. http://dx.doi.org/10.1128/jvi.75.14.6601-6608.2001.

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ABSTRACT Human immunodeficiency virus type 1F12(HIV-1F12) interferes with the replication of other strains of HIV. Its accessory protein, Nef, is sufficient for this phenotype, where the production and infectivity of HIV are impaired significantly. The analysis of three rare mutations in this Nef protein revealed that these effects could be separated genetically. Moreover, the defect in virus production correlated with the lack of processing of the p55Gag precursor in the presence of Nef from HIV-1F12. Importantly, the introduction of one of these mutations (E177G) into Nef from HIV-1NL4-3 also created a dominant-negative Nef protein. Effects of Nef from HIV-1F12on virus production and Gag processing correlated with its altered subcellular distribution. Moreover, the association with two new cellular proteins with molecular masses of 74 and 75 kDa, which do not interact with other Nef proteins, correlated with the decreased virion infectivity. The identification of a dominant-negative protein for the production and infectivity of HIV suggests that Nef plays an active role at this stage of the viral replicative cycle.
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Meschi, Joseph, Erika C. Crouch, Paul Skolnik, Khabirah Yahya, Uffe Holmskov, Rikke Leth-Larsen, Ida Tornoe, Tesfaldet Tecle, Mitchell R. White, and Kevan L. Hartshorn. "Surfactant protein D binds to human immunodeficiency virus (HIV) envelope protein gp120 and inhibits HIV replication." Journal of General Virology 86, no. 11 (November 1, 2005): 3097–107. http://dx.doi.org/10.1099/vir.0.80764-0.

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The envelope protein (gp120) of human immunodeficiency virus (HIV) contains highly conserved mannosylated oligosaccharides. These glycoconjugates contribute to resistance to antibody neutralization, and binding to cell surface lectins on macrophages and dendritic cells. Mannose-binding lectin (MBL) binds to gp120 and plays a role in defence against the virus. In this study it is demonstrated that surfactant protein D (SP-D) binds to gp120 and inhibits HIV infectivity at significantly lower concentrations than MBL. The binding of SP-D was mediated by its calcium-dependent carbohydrate-binding activity and was dependent on glycosylation of gp120. Native dodecameric SP-D bound to HIV gp120 more strongly than native trimeric SP-D. Since one common polymorphic form of SP-D is predominantly expressed as trimers and associated with lower blood levels, these individuals may have less effective innate defence against HIV. A chimeric protein containing the N-terminal and collagen domains of SP-D linked to the neck and carbohydrate-recognition domains of MBL (called SP-D/MBLneck+CRD) had greater ability to bind to gp120 and inhibit virus replication than either SP-D or MBL. The enhanced binding of SP-D/MBLneck+CRD was dependent on assembly into higher molecular mass multimers (i.e. a trimeric form of the chimera did not bind to a greater extent than MBL). Hence, the enhanced binding of SP-D compared with MBL results from distinctive properties of its N-terminal and/or collagen domains. SP-D is present in lung and airway fluids, as well as in blood and various mucosal locations, and could, like MBL, play a role in restricting HIV transmission or replication in vivo.
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Dissertations / Theses on the topic "Protein-HIV Virus"

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Douglas, Chanel Catherine. "A study into the protein/protein interactions involved in HIV-1 capsid assembly." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/douglas.pdf.

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Seckler, James Malcolm. "The Structural Dynamics of Human Immunodeficiency Virus Type I Reverse Transcriptase." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1298562809.

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Apcher, Géraud-Sébastien. "HIV-1 Tat protein and proteasomal Subunit Interactions." Clermont-Ferrand 2, 2003. http://www.theses.fr/2003CLF21470.

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Etant la source centrale de production de peptides antigéniques, le protéasome, un complexe multiprotéique qui est un constituant majeur de la voie protéolytique non-lysosomale, semble être une des cibles principales pour les virus. En réponse à une production d'interféron-y lors d'une infection virale, les nouveaux immunoprotéasomes produisent des peptides provenant de la dégradation de protéines virales qui vont alors interagirent avec les molécules de classes I du CMH afin de déclencher une réponse cytosolique en vue d'éliminer les cellules infectées. La réponse immunitaire cellulaire à une infection par le VIH est inhabituelle. Ce phénomène serait dû à la protéine Tat du VIH. Un des buts précis de ce projet était de démontrer les interactions entre les différentes sous-unités alpha du protéasome 20S qui n'ont pas été prédictes auparavant dans l'étude de la structure crystal du protéasome 20S de levure. A l'aide de la technique du double hybride nous avons pu montrer que la sous-unité alpha7 intéragit fortement avec la sous-unité alpha4 ainsi qu'avec les 5 autres sous-unités alpha. Ces résultats ont été également justifié par l'interaction des sous-unités alpha-radiomarquées, aux protéines de fusions GST-alpha. L'autre but de ce projet était de déterminer quelles sous-unités du protéasome 20S interagissaient avec la protéine Tat. Utilisant la technique de chromatographie d'affinité nous avons pu montrer que la protéine Tat intéragissait avec les sous-unités alpha4 et alpha7 ainsi qu'avec 8 pro-sous-unités bêta. En outre, la protéine Tat inhibe partiellement l'interaction entre ces deux sous-unités. D'autre part la protéine Tat inhibe l'activité chymotrypsine du protéasome 20S in vivo. La protéine Tat peut ainsi, d'une part, interférer avec l'assemblage du protéasome 20S et, d'autre part, inhiber la production de peptides antigéniques et donc leurs présentations aux molécules de classes I des cellules infectées
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Abdurahman, Samir. "Studies on HIV-1 core assembly /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-363-4/.

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Leung, Sze-ki, and 梁詩琪. "Mechanism of human immunodeficiency virus induced immunedysregulation: TAT & IL-18 interaction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B34605472.

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Antonucci, Jenna Marie. "Mechanisms of HIV-1 Restriction by the Host Protein SAMHD1." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1524006072232491.

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Leung, Sze-ki. "Mechanism of human immunodeficiency virus induced immune dysregulation TAT & IL-18 interaction /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34605472.

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Postupalenko, Viktoriia. "Ratiometric fluorophores for peptides and oligonucleotides labeling : application to the HIV-1 nucleocapsid protein." Strasbourg, 2011. https://publication-theses.unistra.fr/public/theses_doctorat/2011/POSTUPALENKO_Viktoriia_2011_ED414.pdf.

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Ce travail porte sur le développement de sondes fluorescentes 3-hydroxychromones pour suivre l’interaction de protéines avec des oligonucléotides (ODNs) et des membranes. Ces sondes ont deux bandes d'émission bien séparées et sensibles à l'environnement, résultant d’un transfert de proton intramoléculaire à l’état excité, d’où une détection des interactions via leur rapport d'intensité. Un analogue d’acide aminé dérivé de la sonde 3HC a été synthétisé puis inséré à des positions ciblées de la protéine de la nucléocapside (NC) du VIH-1. Nous avons ainsi obtenus des informations site-spécifique sur les modifications induites à proximité du site marqué lors de l’interaction avec des ODNs, une alternative étant d’utiliser des nucléosides fluorescents introduits en différentes positions des ODNs. Pour étudier les interactions peptide-membrane, une sonde 3HC sensible aux changements de polarité en solvants apolaires a été couplée à l’extrémité N-terminale de peptides synthétiques (mélittine, magaïnine, poly-L-lysine) connus pour interagir avec les biomembranes. Le rapport d'intensité se corréle bien avec la profondeur d'insertion de cette région N-terminale. Enfin, nous avons appliqué cette sonde pour détecter des interactions possibles de la NC avec les membranes. Nous avons montré que NC se lie avec une forte affinité par voie électrostatique aux membranes contenant des lipides anioniques, permettant de localiser NC au niveau des têtes lipidiques. NC déstabilise la membrane de manière dose-dépendante. Les complexes NC-ADN se lient également aux membranes comme la NC libre, permettant de suggérer une participation de NC à l'import nucléaire du complexe de pré-intégration
This work focuses on the development of a methodology for sensing interactions of proteins with oligonucleotides (ODNs) and membranes based on fluorescent probes from the 3-hydroxychromone (3HC) family. Due to an excited state intramolecular proton transfer, these dyes exhibit two highly resolved emission bands, differently sensitive to the environment, thus allowing to sense interactions through their intensity ratio changes. An amino acid analogue based on 3HC was synthesized and inserted at selected positions of the HIV-1nucleocapsid protein (NC), to further characterize the peptide-ODNs interaction and provide site-specific information on the environmental changes induced by the interaction close to the labeling site. As an alternative, fluorescent nucleosides were synthesized and applied to different positions of ODNs. To study the peptide-membrane interactions, 3HC probe sensitive to polarity changes in apolar solvents was coupled to the N-terminus of melittin, magainin and poly-L-lysine peptides, known to interact with lipid membranes. The observed intensity ratio of the probe correlates well with the insertion depth of the N-terminal region of the peptides. Finally, we applied this dye for the detection of possible interactions of NC with membranes. We have shown that NC binds with high affinity to membranes containing negatively charged lipids. This interaction is mainly driven by electrostatic forces and locates NC at the level of lipid heads. Moreover, NC destabilizes the membrane in a concentration-dependent manner. As free NC, NC-DNA complexes can also bind to membranes, suggesting an involvement of NC in the nuclear import of the pre-integration complex
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Zheng, Yingfeng. "Functional analysis on the interactions of the human immunodeficiency virus type 1 integrase with its cofactors that regulate viral replication." BioMed Central Ltd, 2008. http://hdl.handle.net/1993/16248.

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Like all viruses, the replication of HIV-1 relies heavily on host proteins due to its limited genome products. HIV-1 integrase (IN) catalyzes the integration of viral DNA into host genome and also impacts other steps of viral replication cycle, all of which are assisted by various cellular proteins. Among them, LEDGF/p75 acts as the IN-to-chromatin tethering factor. However, whether other cellular cofactors also participate in this process still remains elusive. To gain insight into the mechanism of action of HIV-1 IN during viral integration, we used a previously described IN/yeast lethality system and our results revealed that the HIV-1 IN-induced yeast lethality absolutely required its chromatin binding ability. Since there is no yeast homolog of LEDGF/p75, it raises the possibility that IN may recruit other cellular cofactors for its chromatin targeting. Consistently, further analysis in mammalian cells indicated that HIV-1 IN was able to mediate chromatin binding independent of IN-LEDGF/p75 interaction and that HIV-1 fitness relied more on chromatin binding than LEDGF/p75 binding of IN. These data greatly enrich our current knowledge on the dynamic interplay within the ternary complex IN/LEDGF/chromatin. HIV-1 exploits multiple cellular cofactors not only to facilitate viral replication, but also to evade the host defense system in favor of the virus. IN is known to be an unstable protein, degraded by the host ubiquitin-proteasome pathway. To investigate how IN avoids the host degradation machinery in the context of viral infection, we showed that IN interacted with host protein Ku70 and protected itself from the Lys48-linked polyubiquitination proteasomal pathway. More importantly, Ku70 was shown to be incorporated into the progeny virus in an IN-dependent manner, and both cell- and virus- associated Ku70 were essential for HIV-1 replication. Finally, the data demonstrated that the interactions between HIV-1 IN and host cofactors can be regulated through its SUMO-interacting motifs (SIMs). Three putative SIMs (72VILV75; 200IVDI203 and 257IKII260) in IN were examined and shown to be essential for IN-LEDGF/p75 but not IN-Ku70 interaction. In summary, this study advances our knowledge of the interaction network between IN and its cofactors, which would have important implications for the design of anti-HIV drugs.
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Zhang, Wei Hong. "Studies on structure and function of human immunodeficiency virus type one (HIV-1) Gag protein." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320175.

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Books on the topic "Protein-HIV Virus"

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Chiu, Simon. The cloning, expression, purification and crystallization of P24, the major core capsid protein of human immunodeficiency virus type (HIV-1). Ottawa: National Library of Canada, 1996.

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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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National Institute of Allergy and Infectious Diseases (U.S.) and National Institutes of Health (U. S.), eds. People who lack a cell surface protein called CCR5 are highly resistant to infection by HIV but may be at increased risk of developing West Nile virus. [Washington, D.C.?]: National Institutes of Health, 2006.

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Spearman, Paul, and Eric O. Freed. HIV Interactions with Host Cell Proteins. Springer Berlin / Heidelberg, 2012.

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Spearman, Paul, and Eric O. Freed. HIV Interactions with Host Cell Proteins. Springer, 2010.

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Book chapters on the topic "Protein-HIV Virus"

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Duesberg, Peter H. "Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV." In AIDS: Virus- or Drug Induced?, 49–68. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1651-7_3.

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Henklein, P., R. Sohr, M. Brudel, R. Pipkorn, and U. Schubert. "Synthesis of the HIV-1 encoded virus protein U." In Peptides 1994, 379–80. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_170.

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Datta, Siddhartha A. K., and Alan Rein. "Preparation of Recombinant HIV-1 Gag Protein and Assembly of Virus-Like Particles In Vitro." In Methods in Molecular Biology, 197–208. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-170-3_14.

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Štrop, P., M. Hořejší, J. Konvalinka, R. Škrabana, J. Velek, I. Bláha, V. Černá, et al. "Protein-Engineered Proteinase of Myeloblastosis Associated Virus, An Enzyme of High Activity and HIV-1 Proteinase-Like Specificity." In Advances in Experimental Medicine and Biology, 515–18. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6012-4_68.

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Ryser, Hugues J. P., Richard Mandel, Angelo Gallina, and Alicia Rivera. "Plasma Membrane Protein Disulfide Isomerase: Its Role in the Translocation of Diphtheria Toxin and HIV Virus Across Endosomal and Cell Membranes." In Plasma Membrane Redox Systems and their Role in Biological Stress and Disease, 279–307. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2695-5_12.

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Wayne, Marta L., and Benjamin M. Bolker. "4. HIV." In Infectious Disease: A Very Short Introduction, 41–53. Oxford University Press, 2015. http://dx.doi.org/10.1093/actrade/9780199688937.003.0004.

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HIV is the human immunodeficiency virus that causes acquired immunodeficiency syndrome, or AIDS. Its transmission is by exchange of bodily fluids. HIV can only enter immune cells with the surface protein gp120. The virus can hide in these cells for many years before it is activated, although it can be transmitted throughout this period. Once activated, the virus begins to replicate, ultimately causing the immune system of the infected person to collapse making them vulnerable to opportunistic infections. ‘HIV’ describes how evolutionary biology has been used to clarify the origins of the epidemic. The rapid mutation rates and recombination that make HIV very hard to treat are also explained. Despite these challenges, a regimen of highly active anti-retroviral therapies (HAART), developed in the mid 1990s, is extraordinarily effective against HIV.
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Miller, Aaron E., Tracy M. DeAngelis, Michelle Fabian, and Ilana Katz Sand. "A Case of Cognitive Change in HIV." In Neuroimmunology, 163–66. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190693190.003.0031.

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Progressive multifocal leukoencephalopathy (PML) is caused by CNS infection with the John Cunningham (JC) virus. It occurs exclusively in patients who are immunosuppressed or under treatment with particular immunomodulatory therapies. Despite advances in antiretroviral therapy (ART), PML remains an issue in HIV patients with drug resistance or with poor access or compliance to ART. PML typically presents with the subacute onset of focal neurological symptoms and/or cognitive/personality changes, dependent upon the location of the lesion(s). MRI usually shows a poorly demarcated T2 hyperintensity, which may or may not enhance with gadolinium. Diffusion restriction is common. CSF profile is typically bland, often with mildly elevated protein. A positive CSF JC virus PCR is diagnostic, but sensitivity is suboptimal, leading to brain biopsy in patients where the diagnosis is not clear. No specific antiviral treatments have been proven effective for the treatment of PML. ART should be initiated or optimized in patients with HIV, as this has been demonstrated to improve outcomes. Some HIV patients treated with ART will develop immune reconstitution inflammatory syndrome (IRIS), which usually is associated with improved prognosis but, in and of itself, may be fatal. Steroid treatment of IRIS remains controversial.
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W. Ryan, Kevin, Randall J. Owens, and Julia L Hurwitz. "Preparation and use of vaccinia virus vectors for HIV protein expression and immunization." In Immunology Methods Manual, 1993–2015. Elsevier, 1996. http://dx.doi.org/10.1016/b978-012442710-5.50225-2.

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WRYAN, K., R. JOWENS, and J. LHURWITZ. "Preparation and use of vaccinia virus vectors for HIV protein expression and immunization." In Immunology Methods Manual, 1993–2015. Elsevier, 1996. http://dx.doi.org/10.1016/b978-012442710-5/50225-2.

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Unissa, Ameeruddin Nusrath, and Luke Elizabeth Hanna. "Dissection of HIV-1 Protease Subtype B Inhibitors Resistance Through Molecular Modeling Approaches." In Big Data Analytics in HIV/AIDS Research, 149–70. IGI Global, 2018. http://dx.doi.org/10.4018/978-1-5225-3203-3.ch007.

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Protease (PR) is an important enzyme required for the posttranslational processing of the viral gene products of type-1 human immunodeficiency virus (HIV-1). Protease inhibitors (PI) act as competitive inhibitors that bind to the active site of PR. The I84V mutation contributes resistance to multiple PIs, and structurally, this mutation affects both sides of the enzyme active site. In order to get insights about this major resistance site to PR inhibitors using in silico approaches, in this chapter, the wild-type (WT) and mutant (MT) I84V of PR were modeled and docked with all PR inhibitors: Atazanavir, Darunavir, Indinavir, Lopinavir, Nelfinavir, Saquinavir, and Tipranavir. Docking results revealed that in comparison to the WT, the binding score was higher for the MT-I84V. Thus, it can be suggested that the high affinity towards inhibitors in the MT could be due to the presence of energetically favorable interactions, which may lead to tight binding of inhibitors with the MT protein, leading to the development of PR resistance against PIs in HIV-1 eventually.
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Conference papers on the topic "Protein-HIV Virus"

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Taveira, Elisa Borges, Marco Fidel Guevara-Vega, Igor Andrade Santos, Douglas Carvalho Caixeta, Victoria Riquena Grosche, Thulio Marquez Cunha, Murillo Guimarães Carneiro, Ana Carolina Gomes Jardim, and Robinson Sabino-Silva. "SARS-CoV-2 structures detection in artificial saliva using ATR-FTIR associated with Linear Discriminant Analysis." In Latin America Optics and Photonics Conference. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/laop.2022.tu1c.8.

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Here, we used ATR-FTIR platform supported by artificial intelligence algorithms to identify unique infrared vibrational modes of a pseudotyped human immunodeficiency virus type-1 (HIV-1) coupled to Spike (S) protein of SARS-CoV-2 (HIV/NanoLuc-SARS-CoV-2 pseudotype virus).
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Barnes, Bradley, Maryam Karimloo, Andrew Schoenrock, Daniel Burnside, Edana Cassol, Alex Wong, Frank Dehne, Ashkan Golshani, and James R. Green. "Predicting novel protein-protein interactions between the HIV-1 virus and homo sapiens." In 2016 IEEE EMBS International Student Conference (ISC). IEEE, 2016. http://dx.doi.org/10.1109/embsisc.2016.7508598.

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Bustamam, A., I. Mujtahidah, and D. Lestari. "Applications of fruit fly optimization algorithm for analyzing protein-protein interaction through Markov clustering on HIV virus." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064228.

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Barrett, P. N., G. Wöber, J. Eibl, and F. Dorner. "EFFICIENCY OF STEAM TREATMENT PROCEDURES USED FOR VIRUS INACTIVATION IN HUMAN COAGULATION FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644152.

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The transmission of viral agents from blood products derived from humanplasma has long been a serious healthproblem for the recipients. The majoragents involved are HBV, nonA nonB, Delta agent and HIV (LAV/HTLV-III). Wehave attempted to design product-specific viral inactivation procedures toprevent such transmission in blood products. Experiments were carried out with HIV, which is the only one of the above viruses which can be propagated and titrated in cell culture, and with a wide range of model viruses. High titre virus was added to blood products, and they were then subjected to different virus inactivation procedures.Heat treatment was carried out in aqueous solution with and without protein-stabilising agents, and it was demonstrated that such agents added toprevent loss of biological activity of blood products also resulted in a stabilisation of contaminating viruses.Therefore steam treatment inactivation procedures have been developed without the addition of such agents. Steam pressure, temperature and time of inactivation are the main variablesand these can be altered for each product to achieve an optimal balance between the degree of virus inactivation and retention of biological activity.It has been shown that each of thedifferent product-specific treatment procedures has a high HIV inactivation capacity.Studies with various model virusesalso demonstrated that the efficiencyof these procedures could be furtherimproved if necessary by altering various parameters such as steam pressure.
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Bustamam, A., M. S. Wisnubroto, and D. Lestari. "Analysis of protein-protein interaction network using Markov clustering with pigeon-inspired optimization algorithm in HIV (human immunodeficiency virus)." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064226.

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Hashim, Uda, M. F. Fatin, A. R. Ruslinda, Subash C. B. Gopinath, and M. N. A. Uda. "Detection of human immunodeficiency virus type 1 (HIV-1) Tat protein by aptamer-based biosensors." In 11TH ASIAN CONFERENCE ON CHEMICAL SENSORS: (ACCS2015). Author(s), 2017. http://dx.doi.org/10.1063/1.4975254.

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Lestari, D., S. Aprilia, and A. Bustamam. "Performance analysis of support vector machine combined with global encoding on detection of protein-protein interaction network of HIV virus." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064225.

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Lestari, D., M. I. S. Musti, and A. Bustamam. "Sequence-based prediction of protein-protein interactions using ensemble based classifier combined with global encoding in HIV (human immunodeficiency virus)." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064227.

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Heimburger, N., P. Fuhge, J. Hilfenhaus, G. Kumpe, and H. E. Karges. "EXPERIMENTAL STUDIES CONCERNING THE VIRUS SAFETY OF PASTEURIZED FIBRINOGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644153.

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Fibrinogen is available for substitution in afibrinogenaemic patientssince about 4 decades. However, it soon turned out that those concentrates bear a high risk of transmitting serum hepatitis. Over many years it was not possible to produce safe concentrates of fibrinogen. Hence, the therapy with this protein was limited to vital indications. We have now succeeded to stabilize fibrinogen inaqueous solution for pasteurization over 10 to 20 hours at 60°C.The efficacy of the virus inactivation was tested using various animal viruses. Following results were obtained.Tests in chimpanzees for hepatitis B safety revealed that this procedure inactivates and eliminates 105.2 CID50 of hepatitis B virus; HIV experiments are going on.By immunizing rabbits with the pasteurized fibrinogen and absorption of the antiserum obtained with the unpasteurized product, an exposition of neoantigens during heating in aqueous solution could be excluded. This result could be further confirmed using passive cutaneous anaphylaxis.The coagulability of the pasteurized fibrinogen is unchanged, compared to not pasteurized material. It iseasily soluble and can be used for both, i. v. infusion and as a tissue adhesive. The clinical tolerability is very good.
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Lestari, D., S. Hartomo, and A. Bustamam. "Sequence-based prediction of protein-protein interactions using pseudo substitution matrix representation features and ensemble rotation forest classifier in HIV (human immunodeficiency virus)." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064224.

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Reports on the topic "Protein-HIV Virus"

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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