Relevant bibliographies by topics / HIV-1 Integrase Inhibitors

Academic literature on the topic 'HIV-1 Integrase Inhibitors'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "HIV-1 Integrase Inhibitors"

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Dayam, Raveendra, Laith Q. Al-Mawsawi, and Nouri Neamati. "HIV-1 Integrase Inhibitors." Drugs in R & D 8, no. 3 (2007): 155–68. http://dx.doi.org/10.2165/00126839-200708030-00003.

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Liao, Chenzhong, Christophe Marchand, Terrence R. Burke Jr, Yves Pommier, and Marc C. Nicklaus. "Authentic HIV-1 integrase inhibitors." Future Medicinal Chemistry 2, no. 7 (July 2010): 1107–22. http://dx.doi.org/10.4155/fmc.10.199.

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Zhao, He, Nouri Neamati, Abhijit Mazumder, Sanjay Sunder, Yves Pommier, and Terrence R. Burke. "Arylamide Inhibitors of HIV-1 Integrase." Journal of Medicinal Chemistry 40, no. 8 (April 1997): 1186–94. http://dx.doi.org/10.1021/jm960449w.

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Neamati, Nouri, Jim A. Turpin, Heather E. Winslow, John L. Christensen, Karen Williamson, Ann Orr, William G. Rice, et al. "Thiazolothiazepine Inhibitors of HIV-1 Integrase." Journal of Medicinal Chemistry 42, no. 17 (August 1999): 3334–41. http://dx.doi.org/10.1021/jm990047z.

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Korolev, S. P., O. V. Kondrashina, D. S. Druzhilovsky, A. M. Starosotnikov, M. D. Dutov, M. A. Bastrakov, I. L. Dalinger, et al. "Structural-Functional Analysis of 2,1,3-Benzoxadiazoles and Their N-oxides As HIV-1 Integrase Inhibitors." Acta Naturae 5, no. 1 (March 15, 2013): 63–72. http://dx.doi.org/10.32607/20758251-2013-5-1-63-72.

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Human immunodeficiency virus type 1 integrase is one of the most attractive targets for the development of anti-HIV-1 inhibitors. The capacity of a series of 2,1,3-benzoxadiazoles (benzofurazans) and their N-oxides (benzofuroxans) selected using the PASS software to inhibit the catalytic activity of HIV-1 integrase was studied in the present work. Only the nitro-derivatives of these compounds were found to display inhibitory activity. The study of the mechanism of inhibition by nitro-benzofurazans/benzofuroxans showed that they impede the substrate DNA binding at the integrase active site. These inhibitors were also active against integrase mutants resistant to raltegravir, which is the first HIV-1 integrase inhibitor approved for clinical use. The comparison of computer-aided estimations of the pharmacodynamic and pharmacokinetic properties of the compounds studied and raltegravir led us to conclude that these compounds show promise and need to be further studied as potential HIV-1 integrase inhibitors.
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Vandegraaff, Nick, Raman Kumar, Helen Hocking, Terrence R. Burke, John Mills, David Rhodes, Christopher J. Burrell, and Peng Li. "Specific Inhibition of Human Immunodeficiency Virus Type 1 (HIV-1) Integration in Cell Culture: Putative Inhibitors of HIV-1 Integrase." Antimicrobial Agents and Chemotherapy 45, no. 9 (September 1, 2001): 2510–16. http://dx.doi.org/10.1128/aac.45.9.2510-2516.2001.

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ABSTRACT To study the effect of potential human immunodeficiency virus type 1 (HIV-1) integrase inhibitors during virus replication in cell culture, we used a modified nested Alu-PCR assay to quantify integrated HIV DNA in combination with the quantitative analysis of extrachromosomal HIV DNA. The two diketo acid integrase inhibitors (L-708,906 and L-731,988) blocked the accumulation of integrated HIV-1 DNA in T cells following infection but did not alter levels of newly synthesized extrachromosomal HIV DNA. In contrast, we demonstrated that L17 (a member of the bisaroyl hydrazine family of integrase inhibitors) and AR177 (an oligonucleotide inhibitor) blocked the HIV replication cycle at, or prior to, reverse transcription, although both drugs inhibited integrase activity in cell-free assays. Quercetin dihydrate (a flavone) was shown to not have any antiviral activity in our system despite reported anti-integration properties in cell-free assays. This refined Alu-PCR assay for HIV provirus is a useful tool for screening anti-integration compounds identified in biochemical assays for their ability to inhibit the accumulation of integrated HIV DNA in cell culture, and it may be useful for studying the effects of these inhibitors in clinical trials.
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Depatureaux, Agnès, Peter K. Quashie, Thibault Mesplède, Yingshan Han, Hannah Koubi, Jean-Christophe Plantier, Maureen Oliveira, Daniela Moisi, Bluma Brenner, and Mark A. Wainberg. "HIV-1 Group O Integrase Displays Lower Enzymatic Efficiency and Higher Susceptibility to Raltegravir than HIV-1 Group M Subtype B Integrase." Antimicrobial Agents and Chemotherapy 58, no. 12 (September 15, 2014): 7141–50. http://dx.doi.org/10.1128/aac.03819-14.

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ABSTRACTHIV-1 group O (HIV-O) is a rare HIV-1 variant characterized by a high number of polymorphisms, especially in the integrase coding region. As HIV-O integrase enzymes have not previously been studied, our aim was to assess the impact of HIV-O integrase polymorphisms on enzyme function and susceptibility to integrase inhibitors. Accordingly, we cloned and purified integrase proteins from each of HIV-1 group O clades A and B, an HIV-O divergent strain, and HIV-1 group M (HIV-M, subtype B), used as a reference. To assess enzymatic function of HIV-O integrase, we carried out strand transfer and 3′ processing assays with various concentrations of substrate (DNA target and long terminal repeats [LTR], respectively) and characterized these enzymes for susceptibility to integrase strand transfer inhibitors (INSTIs) in cell-free assays and in tissue culture, in the absence or presence of various concentrations of several INSTIs. The inhibition constant (Ki) and 50% effective concentration (EC50) values were calculated for HIV-O integrases and HIV-O viruses, respectively, and compared with those of HIV-M. The results showed that HIV-O integrase displayed lower activity in strand transfer assays than did HIV-M enzyme, whereas 3′ processing activities were similar to those of HIV-M. HIV-O integrases were more susceptible to raltegravir (RAL) in competitive inhibition assays and in tissue culture than were HIV-M enzymes and viruses, respectively. Molecular modeling suggests that two key polymorphic residues that are close to the integrase catalytic site, 74I and 153A, may play a role in these differences.
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Suzuki, Shintaro, Emiko Urano, Chie Hashimoto, Hiroshi Tsutsumi, Toru Nakahara, Tomohiro Tanaka, Yuta Nakanishi, et al. "Peptide HIV-1 Integrase Inhibitors from HIV-1 Gene Products." Journal of Medicinal Chemistry 53, no. 14 (July 22, 2010): 5356–60. http://dx.doi.org/10.1021/jm1003528.

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Burke, Terrence R. Jr, Mark Fesen, Abhijit Mazumder, Jessie Yung, Jian Wang, Adelaide M. Carothers, Dezider Grunberger, John Driscoll, Yves Pommier, and Kurt Kohn. "Hydroxylated Aromatic Inhibitors of HIV-1 Integrase." Journal of Medicinal Chemistry 38, no. 21 (October 1995): 4171–78. http://dx.doi.org/10.1021/jm00021a006.

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Neamati, Nouri. "Dipyrimidine-based inhibitors of HIV-1 integrase." Expert Opinion on Investigational Drugs 12, no. 2 (February 2003): 289–92. http://dx.doi.org/10.1517/13543784.12.2.289.

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Dissertations / Theses on the topic "HIV-1 Integrase Inhibitors"

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Jurado, Kellie Ann. "Allosteric Integrase Inhibitors Reveal a Role for Integrase During HIV-1 Maturation." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845485.

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Integration of the DNA copy of the HIV-1 genome is an essential step for virus replication and is mediated by a homotetrameric complex of the viral protein integrase (IN) in association with the ends of linear viral DNA (vDNA). HIV-1 integrates into actively transcribed genes, a trait mediated by cellular host cofactor LEDGF/p75. LEDGF/p75 engages IN in a pocket formed by dimerization of the IN catalytic core domain, a region that has been validated as a drug target for allosteric IN inhibitors (ALLINIs). Previous in vitro work suggested that ALLINIs function through disruption of two integration-associated functions: IN-vDNA complex formation and the IN-LEDGF/p75 interaction. We now demonstrate that ALLINI potency is accounted for during the late phase of HIV-1 replication where the inhibitors block the formation of the viral core, converting the normally electron-dense conical core to an eccentric phenotype where the electron-density exists as a condensate situated between a translucent core and the viral membrane. We have further elucidated the eccentric condensates to represent non-packaged viral ribonucleoprotein (vRNP) complexes and that either genetic or pharmacological inhibition of IN can impair vRNP encapsidation. Supplying IN in trans as part of a Vpr-IN fusion protein partially restored the formation of conical cores with the internal electron density. Moreover the ability of ALLINIs to induce eccentric condensate formation required both IN and viral RNA. Based on these observations, we propose an active role for IN during HIV-1 maturation that involves initiating core morphogenesis and vRNP encapsidation.
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Slaughter, Alison Paige. "Mechanism of action of allosteric HIV-1 integrase inhibitors." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1428684473.

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Omune, Duncan Otieno. "Synthetic analogs of equisetin as potential HIV-1 integrase inhibitors." Diss., Online access via UMI:, 2004. http://wwwlib.umi.com/dissertations/fullcit/3150487.

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Lee, Yi-Chen. "Studies towards the development of novel HIV-1 integrase inhibitors." Thesis, Rhodes University, 2010. http://hdl.handle.net/10962/d1005022.

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The project has focused on the preparation of several series of compounds designed as potential HIV-1 integrase inhibitors. Various 2-nitrobenzaldehydes have been reacted with two activated alkenes, methyl vinyl ketone (MVK) and methyl acrylate, under Baylis-Hillman conditions to afford α-methylene-β-hydroxylalkyl derivatives in moderate to excellent yields. The reactions were conducted using the tertiary amine catalysts, 1,4-diazabicyclo[2.2.2]octane(DABCO) or 3-hydroxyquinuclidine (3-HQ) with chloroform as solvent, and yields were optimised by varying the catalyst, reagent concentrations and the reaction time. Reductive cyclization of the Baylis-Hillman adducts via catalytic hydrogenation, using 10% palladiumon-carbon catalyst in ethanol, afforded quinoline and quinoline N-oxide derivatives. In some cases “acyclic” reduction products were also isolated. Reaction of the Baylis-Hillman MVK adducts with HCl, has resulted in effective nucleophilic (SN’) displacement of the hydroxyl group to afford allylic chloride derivatives. Direct substitution of these chloro derivatives by secondary or primary amines, followed by catalytic hydrogenation gave quinoline derivatives containing a 3-aminomethyl substituent. The Baylis-Hillman ester adducts obtained from reaction with methyl acrylate were treated directly with various amines to give diastereomeric conjugate addition products. Reactions with piperazine gave N,N’-disubstituted piperazine products. The piperidine derivatives have been dehydrated to give cinnamate esters in moderate yields. The products, which have all been satisfactorily characterised by elemental (HRMS) and spectroscopic (1- and 2-D NMR) analysis, constitute a “library” of compounds for in silico and in vitro studies as potential HIV integrase inhibitors.
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Antwi, Janet. "THE DESIGN, SYNTHESIS AND OPTIMIZATION OF ALLOSTERIC HIV-1 INTEGRASE INHIBITORS." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500653561243795.

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Zhao, Zhuojun. "Interactions of HIV-1 integrase and GAG with nucleic acids, cofactors and inhibitors." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1210907804.

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Hoyte, Ashley Christopher. "Molecular Mechanisms for Antiviral Activities and HIV-1 Resistance to Allosteric Integrase Inhibitors." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1543436136541123.

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Nguyen, Hai Le. "HIV-1 minority variants associated with drug resistance to reverse transcriptase and integrase inhibitors and genetic barrier for the development of resistance to integrase inhibitors." Paris 7, 2012. http://www.theses.fr/2012PA077051.

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Les variants minoritaires résistants (VMR) du VIH-1 aux antirétroviraux n'ont pas été étudiés en Thaïlande. Deux groupes de patients dont le génotypage conventionnel n'a pas montré de mutations associées à la résistance ont été inclus dans l'étude: 104 patients récemment infectés, naïfs de traitement antirétro viral et 22 patients en échec de traitement de première ligne par les inhibiteurs non-nucléosidiques de la transcriptase inverse. Les résultats de pyroséquençage ont montré que la prévalence des variants minoritaires Y181C et M184V dans les 2 groupes est faible en Thaïlande. Le rôle des VMR N155H dans la sélection des profils de résistance au raltégravir (RAL) ont été évalué chez des patients multitraités en échec au RAL. Une PCR allèle spécifique (AS-PCR) a été utilisée pour détecter les mutants N155H. La sélection précoce de cette mutation à des niveaux variés n'influence pas la maintenance de cette mutation pendant l'échec en comparaison avec le passage au double mutant Q148H+Q140S, suggérant que ce mutant N155H n'aurait pas de rôle dans la détermination de profils de résistance. La barrière génétique pour l'évolution de la résistance aux inhibiteurs d'intégrase (INIs) a été comparée entre le sous-type B et CRF01-AE du VIH-1 par l'analyse des 66 mutations associées à la résistance aux INIs dans 144 séquences d'intégrase (109 VIH-1 sous-type CRF01-AE et 35 VIH-1 sous-type B) chez des patients naïfs aux INIs. La plupart des positions d'acides aminés étudiées montrent un haut niveau de conservation, ce qui indique la même barrière génétique entre les sous-types CRF01-AE et B
Minority HIV-1 drug resistance bas not been studied in Thailand. Two groups of patients, whose conventional genotyping results showed no drug resistance-associated mutations, were investigated: 104 homosexual men recently infected with HIV-1, naive to antiretroviral treatment and 22 first-line NNRTI-based failures. Pyrosequencing assay was developed to detect and quantify minority Y181C and M184V variants from the patients' plasma samples. 1/104 (0. 96%) and 3/101 (3%) samples were found harboring Y181C and M184V in the group of homosexual men. In patients with first-line treatment failure, one harbored minority Ml84V mutants (4. 5%). Thus, due to such a low prevalence, minority drug résistance test may not be cost-effective for implementing in Thailand. The mechanism of raltegravir (RAL)-resistant evolutions has not been completely elucidated. Because of the emergence of RAL résistance usually initiated with the N155H mutant, we assessed the role of minority N155H-mutated variants in circulating RNA and archived DNA in 5 heavily treated patients experiencing RAL failure and harboring 3 different résistance profiles. No minority N155H-mutated variant was found by allele specific PCR (AS-PCR) in both plasma and whole blood samples collected at baseline and after RAL withdrawal in ail 5 patients. During RAL failure, the mutation N155H was detected at different levels in 3 patients displaying the N155H pathway and gradually declined when the double mutant Q148H+G140S was selected in one patient. In two patients with the Q148H résistance pathway, no N155H variant was identified by AS-PCR in both viral RNA and DNA. The N155H mutants might not play a role in determining different résistance profiles. The genetic barrier, defined by the accumulative number of drug-associated mutations required for the virus to escape drug-selective pressure, is a crucial factor in the development of drug résistance. There are limited data on subtype CRJF01_AE, a predominant isolate in Southeast Asia. The genetic barrier for the evolution of integrase inhibitors (INIs) including RAL, elvitegravir (EVG), and dolutegravir (DTG) résistance was compared between HIV-1 subtypes B and CRF01_AE by analyzing of 66 substitutions associated with INI résistance at 41 amino acid positions in 144 nucleotide sequences (109 HIV-1 subtype CRF01_AE and 35 HIV-1 subtype B) of IN gene derived from INI-naïve patients. Most studied amino acid positions including ail corresponding to RAL and EVG primary mutations show a high degree of conservation, indicating the same genetic barrier between subtypes CRF01_AE and B. Nevertheless, different genetic barriers were observed in two mutations described to be associated with DTG résistance (L101I, A124T) and other five RAL and EVG secondary mutations (V72I, T125K, G140C/S, V201I), which could have an impact on the development of résistance to RAL, EVG, and DTG
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Lei, Xiangyang. "Design, syntheses and biological activities of L-chicoric acid analogues as HIV-1 integrase inhibitors." Fort Worth, Tex. : Texas Christian University, 2006. http://etd.tcu.edu/etdfiles/available/etd-08012006-092058/unrestricted/xlei.pdf.

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Collart, Koenraad M. P. "Synthetic approaches to PNA-containing acridine threading intercalators as potential novel HIV-1 integrase inhibitors." Thesis, Heriot-Watt University, 2010. http://hdl.handle.net/10399/2317.

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The overall objectives of this research were to devise a viable synthetic route to conjugates, in which 9-aminoacridine 4-carboxamide was tethered through its 4- position to peptide nucleic acids (PNAs), and to evaluate their abilities to act as novel inhibitors of HIV-1 integrase (IN). It was reasoned that such compounds could inhibit the process catalysed by IN either directly by binding to the enzyme or indirectly by binding to the proviral DNA substrate through threading intercalation. The first route to these conjugates investigated involved synthesis of the intermediates 9-oxoacridan-4-carboxylic acid and the thyminyl-PNA monomer ethyl ester. Both these compounds were successfully prepared following established literature procedures. In order to explore the conditions required for coupling 9-oxoacridan-4- carboxylic acid and the thyminyl-PNA monomer ethyl ester, a model study was undertaken involving preparation of the known threading intercalator, 9-amino-DACA. Following literature precedence, 9-oxoacridan-4-carboxylic acid was treated first with excess thionyl chloride to yield 9-chloroacridine-4-carboxyl chloride. Subsequently, this was reacted selectively with N,N-dimethylethylenediamine to give 9-chloro- DACA. Finally, treatment of a phenolic solution of 9-chloro-DACA with gaseous ammonia successfully afforded 9-amino-DACA in a 26% over-all yield. Unfortunately, on applying a similar approach for synthesis of the 9-aminoacridine-4- carboxamide PNA conjugate, none of the desired compound could be identified. In a second alternative strategy a number of alkyl-9-oxoacridan-4-carboxylate precursors (methyl, iso-propyl and t-butyl) were synthesised and subsequently activated, via 9-triazolylation, to allow for substitution in the 9 position with benzyl amine. This resulted in the successful synthesis of the iso-propyl- and t-butyl-9- benzylaminoacridine-4-carboxylate intermediates. Subsequent attempts to generate the 4-carboxyl group in both intermediates, via alkyl-ester cleavage, were only successful via a basic hydrolysis of the iso-propyl ester. Unfortunately, attempts to activate the 4- carboxyl group of the resulting 9-benzylaminoacridine-4carboxylic acid via 4-Nhydroxysuccinimide (NHS) ester formation, to enable subsequent substitution in the 4 position with a PNA monomer, were unsuccessful. The nature of the 9-amino substituent was found to be of importance as it was shown that for 9-anilinoacridine-4- carboxylic acid, NHS activation of the 4-carboxyl was successful and led to synthesis iii of a 9-anilinoacridine-4-carboxamide PNA conjugate. This result prompted us to revise our strategy and led to the synthesis of 9-t-Boc- and 9-Alloc-aminoacridine-4- NHS esters that subsequently both were coupled successfully to a thyminyl-PNA monomer. Subsequent deprotection steps for the 9-Alloc protected PNA-acridine conjugate proved to be cumbersome but fortunately, for the t-Boc protected PNAacridine conjugate t-Boc cleavage with TFA followed by an aqueous basic ethyl ester hydrolysis of the PNA monomer’s C-terminus resulted in completion of a 9-step synthetic route (4% over-all yield) towards the target 9-amino-4-PNA-acridine conjugate, 2-(N-(2-(9-aminoacridine-4-carboxamido)ethyl)-2-(thymin-1-yl)acetamido) acetic acid. The IN inhibitory activities of 9-amino-DACA and one intermediate 9-aminoacridinecontaining compound were evaluated in a cell based antiviral assay. Although their absolute potencies of inhibition were in the micromolar range, their novel scaffold warrants their further investigation as potential anti-IN inhibitors
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Books on the topic "HIV-1 Integrase Inhibitors"

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HIV-1 integrase: Mechanism and inhibitor design. Hoboken, N.J: Wiley, 2011.

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Thu, Ye, and Naiel Nassar. HIV-1 Resistance to Antiretroviral Drugs. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0021.

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Numerous epidemiologic studies of antiretroviral resistance in both treatment-experienced and treatment-naive individuals have been performed in the potent combination antiretroviral therapy (ART) era. The development of antiretroviral resistance depends on previous antiretroviral exposure, compliance with the medication, and availability of a fully active antiretroviral regimen for the individual patient. The previous exposure to ART medications plays significant role in developing drug resistance, especially in patients who are noncompliant with medications. Drug resistance testing should be done in the setting of treatment failure because it can help achieve better virologic response. There is extensive cross-resistance with first-generation non-nucleoside reverse transcriptase inhibitors and first-generation integrase strand inhibitors.
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Majid, Adrian, and Bruce L. Gilliam. Future Antiretrovirals, Immune-Based Strategies, and Therapeutic Vaccines. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0023.

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Highly active antiretroviral therapy remains the mainstay of treatment for patients chronically infected with HIV. Novel drugs, both within existing classes and new ones, are in various stages of development and testing. New medications within existing classes of antiretroviral agents are in clinical trials and will likely offer activity against resistant HIV-1 strains and provide alternatives for combination pill therapy. Novel therapeutics including oral attachment inhibitors and monoclonal antibody treatments continue to show efficacy against HIV-1 and progress in clinical trials. Tenofovir alafenamide is a prodrug that produces higher intracellular levels of tenofovir diphosphate with likely less renal and bone toxicity. Among traditional classes of HIV treatment, both doravirine (a non-nucleoside reverse transcriptase inhibitor) and cabotegravir (an integrase strand inhibitor) are newer agents with activity against resistant virus. Maturation inhibitors are a new class of treatment that block protease cleavage, leading to the release of an immature virion.
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Young, Benjamin. Classes of Antiretrovirals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0019.

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Results of the randomized, international INSIGHT START clinical trial provide definitive proof of the benefit of antiretroviral therapy initiation in asymptomatic individuals with CD4+ counts greater than 500 cells/mm3. There are six different classes of antiretroviral agents: two types of reverse transcriptase inhibitors, two types of entry inhibitors, one class of inhibitors of HIV protease, and one class of inhibitors of HIV integrase. Combination antiretroviral therapy is recommended for all people living with HIV. The primary goal of combination antiretroviral therapy is to achieve viral suppression. Each antiretroviral class targets a unique step in the replication cycle of HIV-1.
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Book chapters on the topic "HIV-1 Integrase Inhibitors"

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Mouscadet, Jean-François, Eric Deprez, Didier Desmaele, and Jean D'Angelo. "Development of Styrylquinoline Integrase Inhibitors." In HIV-1 Integrase, 325–39. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch22.

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Fardis, Maria, Haolun Jin, Xiaowu Chen, Manuel Tsiang, James Chen, Choung Kim, and Matthew Wright. "Conformationally Constrained Tricyclic HIV Integrase Inhibitors." In HIV-1 Integrase, 239–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch16.

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Nair, Vasu, and Guochen Chi. "Nucleotide-Based Inhibitors of HIV Integrase." In HIV-1 Integrase, 379–88. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch25.

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Hombrouck, Anneleen, Reginald Clayton, Arnout Voet, Myriam Witvrouw, and Zeger Debyser. "Resistance to Inhibitors of HIV-1 Integrase." In HIV-1 Integrase, 477–98. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch30.

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Plewe, Michael B., and Ted W. Johnson. "Azaindole Hydroxamic Acids are HIV-1 Integrase Inhibitors." In HIV-1 Integrase, 265–74. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch18.

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Crosby, David C., and W. Edward Robinson. "Dicaffeoyltartaric Acid and Dicaffeoylquinic Acid HIV Integrase Inhibitors." In HIV-1 Integrase, 341–62. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch23.

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Long, Ya-Qiu, and Nouri Neamati. "Design and Discovery of Peptide-Based HIV-1 Integrase Inhibitors." In HIV-1 Integrase, 363–77. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch24.

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Serrao, Erik, Rambabu Gundla, Jinxia Deng, Srinivas Odde, and Nouri Neamati. "Computer-Aided Techniques in Design of HIV-1 Integrase Inhibitors." In HIV-1 Integrase, 389–413. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch26.

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Garvey, Edward P., and Benjamin Schwartz. "Slow-Onset Kinetics of HIV Integrase Inhibitors and Proposed Molecular Model." In HIV-1 Integrase, 255–63. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch17.

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Singh, Sheo B. "Discovery and Development of Natural Product Inhibitors of HIV-1 Integrase." In HIV-1 Integrase, 309–23. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015377.ch21.

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Conference papers on the topic "HIV-1 Integrase Inhibitors"

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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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Masso, Majid. "Fast and Accurate Structure-Based Prediction of Resistance to the HIV-1 Integrase Inhibitor Raltegravir." In BCB'13: ACM-BCB2013. New York, NY, USA: ACM, 2013. http://dx.doi.org/10.1145/2506583.2506703.

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Andonie, R., L. Fabry-Asztalos, S. Abdul-Wahid, C. J. Collar, and N. Salim. "An Integrated Soft Computing Approach for Predicting Biological Activity of Potential HIV-1 Protease Inhibitors." In The 2006 IEEE International Joint Conference on Neural Network Proceedings. IEEE, 2006. http://dx.doi.org/10.1109/ijcnn.2006.246874.

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Zhu, Haiyan, Xuanhe Tang, Maurice B. Dusseault, and John D. McLennan. "What Can We Learn From the Child/Infill Well Fracturing in Shale Gas Reservoir? Some Interesting Insights." In International Geomechanics Symposium. ARMA, 2022. http://dx.doi.org/10.56952/igs-2022-106.

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Abstract:
Abstract Infill horizontal wells with fracturing treatment are being widely applied to enhance the recovery from shale gas reservoirs in Sichuan basin. Frac-hits are commonly treated as a hazard for the adjacent (infill) well production and wellbore. During the infill well fracturing of the gas shale in Sichuan basin, an interesting field phenomenon has been reported: (i) the number of microseismic (MS) events close to the boundary of the parent well SRV decreases sharply. It seems that there is a barrier or a local attenuation process that inhibits significant MS activity from developing within the parent well SRV. (ii) After infill well fracturing, a transitory pressure and production regain were detected in the adjacent parent well. In this work, an integrated flow-geomechanics coupling model has been built, which includes the parent well fracturing, parent well production, infill well fracturing and production. Involving with the field researches in North America, two cases in Fuling gas shale are discussed. The first case is based on an infill well in one main productive layer, while the second case is based on a multi-layer infill wells zone. Mechanism of the field phenomenon from Fuling gas shale infill wells are investigated by the integrated flow-geomechanics coupling model and evidenced by field data. Finally, several inspirations were proposed: (1) Only in gas shale (ultra-low permeable and naturally fractured reservoir)? (2) More geomechanical mechanisms for the MSEB effect? (3) Frac-hit is good or bad? How can we utilize it? More investigations are expected from scholars in different researching fields. Background The well production and pressure of shale gas reservoirs in Sichuan basin (Fuling, Changning, etc) drops over 90% and 75% in two years. Infill horizontal wells with fracturing treatment are being widely applied to enhance recovery from this reservoir.
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