Relevant bibliographies by topics / Viral Drug Resistance

Contents

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

Academic literature on the topic 'Viral Drug Resistance'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Viral Drug Resistance"

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Richman, Douglas D. "Viral drug resistance." Current Opinion in Infectious Diseases 3, no. 6 (December 1990): 819–23. http://dx.doi.org/10.1097/00001432-199012000-00014.

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McKeegan, Kenneth S., M. Ines Borges-Walmsley, and Adrian R. Walmsley. "Microbial and viral drug resistance mechanisms." Trends in Microbiology 10, no. 10 (October 2002): s8—s14. http://dx.doi.org/10.1016/s0966-842x(02)02429-0.

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de Koning, Harry P. "Drug resistance in protozoan parasites." Emerging Topics in Life Sciences 1, no. 6 (December 22, 2017): 627–32. http://dx.doi.org/10.1042/etls20170113.

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As with all other anti-infectives (antibiotics, anti-viral drugs, and anthelminthics), the limited arsenal of anti-protozoal drugs is being depleted by a combination of two factors: increasing drug resistance and the failure to replace old and often shamefully inadequate drugs, including those compromised by (cross)-resistance, through the development of new anti-parasitics. Both factors are equally to blame: a leaking bathtub may have plenty of water if the tap is left open; if not, it will soon be empty. Here, I will reflect on the factors that contribute to the drug resistance emergency that is unfolding around us, specifically resistance in protozoan parasites.
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Endy, Drew, and John Yin. "Toward Antiviral Strategies That Resist Viral Escape." Antimicrobial Agents and Chemotherapy 44, no. 4 (April 1, 2000): 1097–99. http://dx.doi.org/10.1128/aac.44.4.1097-1099.2000.

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ABSTRACT We studied the effect on viral growth of drugs targeting different virus functions using a computer simulation for the intracellular growth of bacteriophage T7. We found that drugs targeting components of negative-feedback loops gain effectiveness against mutant viruses that attenuate the drug-target interaction. The greater inhibition of such mutants than of the wild type suggests a drug design strategy that would hinder the development of drug resistance.
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Kurt Yilmaz, Nese, Ronald Swanstrom, and Celia A. Schiffer. "Improving Viral Protease Inhibitors to Counter Drug Resistance." Trends in Microbiology 24, no. 7 (July 2016): 547–57. http://dx.doi.org/10.1016/j.tim.2016.03.010.

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Menendez-Arias, Luis, and Jose Este. "HIV-Resistance to Viral Entry Inhibitors." Current Pharmaceutical Design 10, no. 15 (June 1, 2004): 1845–60. http://dx.doi.org/10.2174/1381612043384574.

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Schiffer, Celia. "Combatting Drug Resistance: Lessons from the viral proteases of HIV and HCV." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C116. http://dx.doi.org/10.1107/s2053273314098830.

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Drug resistance negatively impacts the lives of millions of patients and costs our society billions of dollars by limiting the longevity of many of our most potent drugs. Drug resistance can be caused by a change in the balance of molecular recognition events that selectively weakens inhibitor binding but maintains the biological function of the target. To reduce the likelihood of drug resistance, a detailed understanding of the target's function is necessary. Both structure at atomic resolution and evolutionarily constraints on its variation is required. "Resilient" targets are less susceptible to drug resistance due to their key location in a particular pathway. This rationale was derived through crystallographic studies elucidating substrate recognition and drug resistance in HIV-1 protease and Hepatitis C (HCV) NS3/4A protease. Both are key therapeutic targets and are potentially "resilient" targets where resistant mutations occur outside of the substrate binding site. To reduce the probability of drug resistance inhibitors should be designed to fit within what we define as the "substrate envelope". These principals are likely more generally applicable to other quickly evolving diseases where drug resistance is quickly evolving. http://www.umassmed.edu/schifferlab/index.aspx
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Raugi, Dana N., Robert S. Nixon, Sally Leong, Khadim Faye, Jean Phillipe Diatta, Fatima Sall, Robert A. Smith, et al. "HIV-2 Drug Resistance Genotyping from Dried Blood Spots." Journal of Clinical Microbiology 59, no. 1 (October 14, 2020): e02303-20. http://dx.doi.org/10.1128/jcm.02303-20.

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ABSTRACTThe treatment of HIV-2 in resource-limited settings (RLS) is complicated by the limited availability of HIV-2-active antiretroviral drugs and inadequate access to HIV-2 viral load and drug resistance testing. Dried blood spots (DBS)-based drug resistance testing, widely studied for HIV-1, has not been reported for HIV-2 and could present an opportunity to improve care for HIV-2-infected individuals. We selected 150 DBS specimens from ongoing studies of antiretroviral therapy (ART) for HIV-2 infection in Senegal and subjected them to genotypic drug resistance testing. Total nucleic acid was extracted from DBS, reverse transcribed, PCR amplified, and analyzed by population-based Sanger sequencing, and major drug resistance-associated mutations (RAM) were identified. Parallel samples from plasma and peripheral blood mononuclear cells (PBMC) were also genotyped. We obtained 58 protease/reverse transcriptase genotypes. Plasma viral load was significantly correlated with genotyping success (P < 0.001); DBS samples with corresponding plasma viral load >250 copies/ml had a success rate of 86.8%. In paired DBS-plasma genotypes, 83.8% of RAM found in plasma were also found in DBS, and replicate DBS genotyping revealed that a single test detected 86.7% of known RAM. These findings demonstrate that DBS-based genotypic drug resistance testing for HIV-2 is feasible and can be deployed in RLS with limited infrastructure.
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Beljanski, Vladimir, Cindy Chiang, and John Hiscott. "The intersection between viral oncolysis, drug resistance, and autophagy." Biological Chemistry 396, no. 12 (December 1, 2015): 1269–80. http://dx.doi.org/10.1515/hsz-2015-0147.

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Abstract Resistance to both cytotoxic and targeted therapies is a major problem facing cancer treatment. The mechanisms of resistance to unrelated drugs share many common features, including up-regulation of detoxifying pathways, activation of pro-survival mechanisms, and ineffective induction of cell death. Oncolytic viruses (OVs) are promising biotherapeutics for cancer treatment that specifically replicate in and lyse cancer cells. In addition to direct viral lysis, the anti-tumor effects of OVs are mediated via innate and adaptive immune responses, and several adaptation mechanisms such as autophagy appear to contribute to their anti-tumor properties. Autophagy is a versatile pathway that plays a key role in cancer survival during stressful conditions such as starvation or cytotoxic drug challenges. Autophagy also plays a role in mediating innate and adaptive immune responses by contributing to antigen presentation and cytokine secretion. This role of autophagy in regulation of immune responses can be utilized to design therapeutic combinations using approaches that either stimulate or block autophagy to potentiate therapeutic efficacy of OVs. Additional studies are needed to determine optimal multimodal combination approaches that will facilitate future successful clinical implementation of OV-based therapies.
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Neagu, Iulia A., Jason Olejarz, Mark Freeman, Daniel I. S. Rosenbloom, Martin A. Nowak, and Alison L. Hill. "Life cycle synchronization is a viral drug resistance mechanism." PLOS Computational Biology 14, no. 2 (February 15, 2018): e1005947. http://dx.doi.org/10.1371/journal.pcbi.1005947.

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Dissertations / Theses on the topic "Viral Drug Resistance"

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Lin, Kuan-Hung. "Viral Proteases as Drug Targets and the Mechanisms of Drug Resistance: A Dissertation." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/841.

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Viral proteases have been shown to be effective targets of anti-viral therapies for human immunodeficiency virus (HIV) and hepatitis C virus (HCV). However, under the pressure of therapy including protease inhibitors, the virus evolves to select drug resistance mutations both in the protease and substrates. In my thesis study, I aimed to understand the mechanisms of how this protease−substrate co-evolution contributes to drug resistance. Currently, there are no approved drugs against dengue virus (DENV); I investigated substrate recognition by DENV protease and designed cyclic peptides as inhibitors targeting the prime site of dengue protease. First, I used X-ray crystallography and subsequent structural analysis to investigate the molecular basis of HIV-1 protease and p1-p6 substrate coevolution. I found that co-evolved p1-p6 substrates rescue the HIV-1 I50V protease’s binding activity by forming more van der Waals contacts and hydrogen bonds, and that co-evolution restores the dynamics at the active site for all three mutant substrates. Next, I used aprotinin as a platform to investigate DENV protease–substrate recognizing pattern, which revealed that the prime side residues significantly modulate substrate affinity to protease and the optimal interactions at each residue position. Based on these results, I designed cyclic peptide inhibitors that target the prime site pocket of DENV protease. Through optimizing the length and sequence, the best inhibitor achieved a 2.9 micromolar Ki value against DENV3 protease. Since dengue protease does not share substrate sequence with human serine proteases, these cyclic peptides can be used as scaffolds for inhibitor design with higher specificity.
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Lin, Kuan-Hung. "Viral Proteases as Drug Targets and the Mechanisms of Drug Resistance: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/841.

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Viral proteases have been shown to be effective targets of anti-viral therapies for human immunodeficiency virus (HIV) and hepatitis C virus (HCV). However, under the pressure of therapy including protease inhibitors, the virus evolves to select drug resistance mutations both in the protease and substrates. In my thesis study, I aimed to understand the mechanisms of how this protease−substrate co-evolution contributes to drug resistance. Currently, there are no approved drugs against dengue virus (DENV); I investigated substrate recognition by DENV protease and designed cyclic peptides as inhibitors targeting the prime site of dengue protease. First, I used X-ray crystallography and subsequent structural analysis to investigate the molecular basis of HIV-1 protease and p1-p6 substrate coevolution. I found that co-evolved p1-p6 substrates rescue the HIV-1 I50V protease’s binding activity by forming more van der Waals contacts and hydrogen bonds, and that co-evolution restores the dynamics at the active site for all three mutant substrates. Next, I used aprotinin as a platform to investigate DENV protease–substrate recognizing pattern, which revealed that the prime side residues significantly modulate substrate affinity to protease and the optimal interactions at each residue position. Based on these results, I designed cyclic peptide inhibitors that target the prime site pocket of DENV protease. Through optimizing the length and sequence, the best inhibitor achieved a 2.9 micromolar Ki value against DENV3 protease. Since dengue protease does not share substrate sequence with human serine proteases, these cyclic peptides can be used as scaffolds for inhibitor design with higher specificity.
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Wilbe, Karin. "Genetic dynamics of HIV-1: recombination, drug resistance and intrahost evolution /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-959-5/.

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Ozen, Aysegul. "Structure and Dynamics of Viral Substrate Recognition and Drug Resistance: A Dissertation." eScholarship@UMMS, 2005. http://escholarship.umassmed.edu/gsbs_diss/677.

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Drug resistance is a major problem in quickly evolving diseases, including the human immunodeficiency (HIV) and hepatitis C viral (HCV) infections. The viral proteases (HIV protease and HCV NS3/4A protease) are primary drug targets. At the molecular level, drug resistance reflects a subtle change in the balance of molecular recognition; the drug resistant protease variants are no longer effectively inhibited by the competitive drug molecules but can process the natural substrates with enough efficiency for viral survival. Therefore, the inhibitors that better mimic the natural substrate binding features should result in more robust inhibitors with flat drug resistance profiles. The native substrates adopt a consensus volume when bound to the enzyme, the substrate envelope. The most severe resistance mutations occur at protease residues that are contacted by the inhibitors outside the substrate envelope. To guide the design of robust inhibitors, we investigate the shared and varied properties of substrates with the protein dynamics taken into account to define the dynamic substrate envelope of both viral proteases. The NS3/4A dynamic substrate envelope is compared with inhibitors to detect the structural and dynamic basis of resistance mutation patterns. Comparative analyses of substrates and inhibitors result in a solid list of structural and dynamic features of substrates that are not shared by inhibitors. This study can help guiding the development of novel inhibitors by paying attention to the subtle differences between the binding properties of substrates versus inhibitors.
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Ozen, Aysegul. "Structure and Dynamics of Viral Substrate Recognition and Drug Resistance: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/677.

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Drug resistance is a major problem in quickly evolving diseases, including the human immunodeficiency (HIV) and hepatitis C viral (HCV) infections. The viral proteases (HIV protease and HCV NS3/4A protease) are primary drug targets. At the molecular level, drug resistance reflects a subtle change in the balance of molecular recognition; the drug resistant protease variants are no longer effectively inhibited by the competitive drug molecules but can process the natural substrates with enough efficiency for viral survival. Therefore, the inhibitors that better mimic the natural substrate binding features should result in more robust inhibitors with flat drug resistance profiles. The native substrates adopt a consensus volume when bound to the enzyme, the substrate envelope. The most severe resistance mutations occur at protease residues that are contacted by the inhibitors outside the substrate envelope. To guide the design of robust inhibitors, we investigate the shared and varied properties of substrates with the protein dynamics taken into account to define the dynamic substrate envelope of both viral proteases. The NS3/4A dynamic substrate envelope is compared with inhibitors to detect the structural and dynamic basis of resistance mutation patterns. Comparative analyses of substrates and inhibitors result in a solid list of structural and dynamic features of substrates that are not shared by inhibitors. This study can help guiding the development of novel inhibitors by paying attention to the subtle differences between the binding properties of substrates versus inhibitors.
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Lockbaum, Gordon J. "Molecular Mechanisms of Resistance and Structure-Based Drug Design in Homodimeric Viral Proteases." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1072.

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Drug resistance is a global health threat costing society billions of dollars and impacting millions of lives each year. Current drug design strategies are inadequate because they focus on disrupting target activity and not restricting the evolutionary pathways to resistance. Improved strategies would exploit the structural and dynamic changes in the enzyme–inhibitor system integrating data from many inhibitors and variants. Using HIV-1 protease as a model system, I aimed to elucidate the underlying resistance mechanisms, characterize conserved protease-inhibitor interactions, and generate more robust inhibitors by applying these insights. For primary mechanisms of resistance, comparing interactions at the protease–inhibitor interface showed how specific modifications affected potency. For mutations distal to the active site, molecular dynamics simulations were necessary to elucidate how changes propagated to reduce inhibitor binding. These insights informed inhibitor design to improve potency against highly resistant variants by optimizing hydrogen bonding. A series of hybrid inhibitors was also designed that showed excellent potency by combining key moieties of multiple FDA-approved inhibitors. I characterized the structural basis for alterations in binding affinity in HIV-1 protease both from mutations and inhibitors. I applied these strategies to HTLV-1 protease, a potential drug target. I identified the HIV-1 inhibitor darunavir as a viable scaffold and evaluated analogues, leading to a low-nanomolar compound with potential for optimization. Hopefully, insights from this thesis will lead to the development of potent HTLV-1 protease inhibitors. More broadly, these inhibitor design strategies are applicable to other rapidly evolving targets, thereby reducing drug resistance rates in the future.
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Svedhem, Johansson Veronica. "Kinetics of HIV-1 drug resistance mutations in vivo /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-671-9/.

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Pugach, Pavel. "The evolutionary response of the HIV-1 ENV complex to selection pressures in vitro /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1428842531&sid=4&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Zephyr, Jacqueto. "Robust Drug Design Strategies and Discovery Targeting Viral Proteases." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1157.

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Viral proteases play crucial roles in the life cycle and maturation of many viruses by processing the viral polyprotein after translation and in some cases cleaving host proteins associated with the immune response. The essential role of viral proteases makes them attractive therapeutic targets. In this thesis, I provide an introductory summary of viral proteases, their structure, mechanism, and inhibition, while the breadth of this thesis focuses on the Hepatitis C virus (HCV) NS3/4A and Zika virus (ZIKV) NS2B/NS3 viral proteases. HCV NS3/4A protease inhibitors (PIs) have become a mainstay in combination therapies. However, drug resistance remains a major problem against these PIs. In this thesis, I applied insights from the HCV substrate envelope (SE) model to develop strategies for designing PIs that are less susceptible to resistance. Also, I used the HCV NS3/4A protease as a model system to decipher the molecular mechanism and role of fluorination in HCV PIs potency and drug resistance. The drug design strategies described in this thesis have broad applications in drug design. The ZIKV is an emerging global threat, and currently, with no treatment available. In this thesis, I described the discovery, biochemical and antiviral evaluation of novel noncompetitive quinoxaline-based inhibitors of the ZIKV NS2B/NS3 protease. The inhibitors are proposed to interfere with NS2 binding to NS3, thereby preventing the protease from adopting the closed and active conformation. The inhibitors from this work will serve as lead compounds for further inhibitor development toward the goal of developing antivirals.
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Malik, S. "The role of the HIV-1 reverse transcriptase mutation H208Y to drug resistance and viral fitness." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1207313/.

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Accessory mutations are thought to arise alongside major or primary drug resistance mutations in order to augment resistance, restore viral fitness, or both. The H208Y mutation in the HIV-1 reverse transcriptase (RT) gene was hypothesised to be an accessory mutation. This thesis characterises the H208Y mutation in terms of linkage of H208Y to other major and accessory resistance mutations, and examines two phenotypic aspects, drug susceptibility and viral fitness. The HIV Resistance Database held at the Royal Free Hospital was searched for genotypes containing the H208Y mutation. The prevalence of H208Y in antiretroviral treatment naïve and treatment experienced patients was 5/3783 (0.1%) and 12/1304 (0.9%), respectively, indicating a high degree of conservation of position 208 in wild type virus and an increase in prevalence under selective drug pressure. Four patients were chosen to conduct further analysis of virus with H208Y, comprising a treatment naïve patient with subtype B virus, and three treatment experienced patients harbouring subtype A, subtype B and subtype C virus respectively. The RT gene from these patients was cloned and sequenced. H208Y was found to be associated with the thymidine analogue mutations (TAMs), particularly mutations at positions D67, T215 and K219. H208Y was always associated with accessory mutations at positions V35, K122 and T200. Recombinant viruses containing patient derived RT genes with and without H208Y were constructed to examine the impact of H208Y on drug susceptibility and viral fitness. A multiple cycle drug susceptibility assay showed that H208Y conferred a reduced susceptibility to the nucleotide RT inhibitor tenofovir in the context of subtype B wild type RT and subtype B RT containing TAMs. Growth competition assays were used to examine the fitness effects of H208Y using allele-specific PCR to differentiate between competing strains with and without H208Y. In the context of subtype B wild type RT, H208Y conferred a reduced viral fitness both in the presence and absence of drug. The effect may be proposed to contribute to the overall high degree of conservation of position 208. In contrast, H208Y did not appear to impact on viral fitness in the context of subtype B and subtype A RT containing TAMs.
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Books on the topic "Viral Drug Resistance"

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Zumla, Alimuddin, David S. C. Hui, and Wing-Wai Yew. Emerging respiratory infections in the 21st century. Philadelphia, PA: Saunders, 2010.

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G, Shekelle Paul, Southern California Evidence-Based Practice Center/RAND., and United States. Agency for Healthcare Research and Quality., eds. Antiretroviral (ARV) drug resistance in the developing world. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Healthcare Research and Quality, 2007.

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(Editor), R. F. Schinazi, J. P. Sommadossi (Editor), and C. Rice (Editor), eds. Frontiers in Viral Hepatitis. Elsevier Science, 2003.

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Gendelman, Howard E., Igor Grant, Ian Paul Everall, Howard S. Fox, Harris A. Gelbard, Stuart A. Lipton, and Susan Swindells, eds. The Neurology of AIDS. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195399349.001.0001.

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This resource discusses how neurological complications of progressive HIV-1 infection remain a common cause of morbidity even during widespread use of antiretroviral therapy (ART). It addresses how long-term resistance to ART, drug compliance, untoward drug side effects, a myriad of opportunistic infection, depression and other psychiatric disease manifestations, concomitant drug abuse, neuropathies, and an inability to clear viral reservoirs, explain, in large measure, disease progression and immune deterioration. It then covers the association with a number of psychiatric, muscle, nerve, infectious, as well as cognitive, behavioral, and motor disturbances seen in infected people, with a focus on the neurological complications, molecular and viral disease processes, cellular factors influencing viral replication therapeutic challenges, and the changing epidemiological patterns of disease.
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Iversen, Les. 3. Drugs as medicines. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198745792.003.0003.

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‘Drugs as medicines’ highlights the principles behind the successful use of medicines to cure or ameliorate the symptoms of many illnesses. These range from infectious diseases, such as bacterial and viral infections; innate conditions, such as mental illness or autoimmune disorders; or those caused by lifestyle, such as coronary heart disease. Despite successes, problems still remain. Many bacteria and viruses are rapidly evolving resistance to drug strategies. Also, those in the developing world, who are most at risk from infection, often benefit least from drugs due to prohibitive costs and reduced investment in treatment. One of the most important medical advances in the past one hundred years has been the contraceptive pill.
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Thursfield, Rebecca, Chris Orchard, Rosanna Featherstone, and Jane C. Davies. Future treatments. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0013.

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There are only a relatively limited armoury of drugs, the majority of which are aimed at downstream symptoms of cystic fibrosis. Therapies targeting the basic defect in CF as well as continued availability of more conventional drugs are required. Progress in gene therapy has been limited by the significant barriers to gene transfer of the CF lung, but the UK is hosting a large repeated dose trial of nebulized non-viral gene therapy designed around clinically meaningful outcomes. The UK CF Gene Therapy Consortium is also seeking to develop a promising modified lentiviral approach, although this is some years off. Perhaps the exciting development of recent decades has come from small molecule CFTR modulators, driven by an understanding of basic pathophysiological mechanisms. Ivacaftor is the first drug to be licensed, having proved itself highly clinically efficacious in patients with the class-3 gating mutation G551D. The trial pipeline seeks to expand indications for this and to explore the potential of Phe508del correctors. Finally, a number of anti-inflammatory and anti-infective strategies are being pursued. The emerging global problem of antibiotic resistance is leading to exciting alternatives such as biofilm disruption and bacteriophage to be explored.
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Buhner, Stephen Harrod. Herbal Antivirals: Natural Remedies for Emerging and Resistant Viral Infections. Storey Publishing, LLC, 2013.

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Herbal antivirals: Natural remedies for emerging resistant and epidemic viral infections. 2013.

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Al-Darraji, Haider A., and Frederick L. Altice. The Perfect Storm. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199374847.003.0008.

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Globally, tuberculosis (TB) is a major cause of morbidity and mortality among people who use drugs (PWUD), particularly those co-infected with HIV. This chapter describes how TB is prevalent in several prison systems by virtue of the concentration of PWUD and people living with HIV. TB is further amplified within this system through overcrowding, poor ventilation, and delayed access to quality prevention and treatment services. In many countries, individuals cycling through prisons are inadequately screened and treated for TB, and affected individuals may have frequent treatment interruptions. For PWUD, relapse to drug use immediately after release from custody can impede continuity of care, which may contribute to the development of drug-resistant TB. Particularly in countries with high incarceration rates, prisons act as amplifiers of TB and drug-resistant TB in the community. The World Health Organization’s recommendations for integration of TB, HIV, and addiction treatment are seldom achieved, especially within prisons. Other factors contributing to poor TB outcomes among PWUD interfacing with prisons include insufficient support to promote medication adherence and co-morbidities, like viral hepatitis that potentiate hepatic toxicity, both of which are prevalent among PWUD.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Vasopressors and Inotropes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0012.

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Vasopressors and inotropes are used in the neurosciences intensive care unit to treat hypotension and to augment blood pressure. Hypotension can be attributed to abnormal cardiac output, abnormal intravascular volume or abnormal systemic vascular resistance. Vasopressors are needed to manage hemodynamic augmentation in patients with severe cerebral vasospasm and aneurysmal subarachnoid hemorrhage, in patients with critical carotid or basilar artery stenosis producing marginal blood flow, or when patients are maintained in drug-induced comas. The main incentive is to maintain adequate perfusion pressure to the brain and vital organs, particularly the kidneys. This chapter provides the essentials of management of these complex drugs and how to avoid unintended side effects.
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Book chapters on the topic "Viral Drug Resistance"

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Reeves, Jacqueline D., and Neil T. Parkin. "Viral Phenotypic Resistance Assays." In Antimicrobial Drug Resistance, 1389–407. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47266-9_35.

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Parkin, Neil. "Viral Phenotypic Resistance Assays." In Antimicrobial Drug Resistance, 1187–99. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8_37.

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Liaqat, Atif, Muhammad Farhan Jahangir Chughtai, Adnan Khaliq, Tariq Mehmood, Samreen Ahsan, Kanza Saeed, Syed Junaid Ur Rahman, et al. "Drugs Resistance Against Viral Diseases." In Biochemistry of Drug Resistance, 57–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-76320-6_3.

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Han, Ying-Shan, and Mark A. Wainberg. "Genotypic Assays for Monitoring Drug Resistance in HIV-1 Infection and for Other Chronic Viral Diseases." In Antimicrobial Drug Resistance, 1501–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47266-9_38.

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Martinez-Cajas, Jorge L., Marco Petrella, and Mark A. Wainberg. "The Use of Genotypic Assays for Monitoring the Development of Resistance to Antiviral Therapy for HIV-1 Infection and Other Chronic Viral Diseases." In Antimicrobial Drug Resistance, 1249–64. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8_40.

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Lloyd, Alun, and Dominik Wodarz. "Drug resistance in acute viral infections: Rhinovirus as a case study." In Disease Evolution, 193–212. Providence, Rhode Island: American Mathematical Society, 2006. http://dx.doi.org/10.1090/dimacs/071/10.

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Lao, Thuan Duc, Hung Chi Lieu, Thuy Thanh Thi Ho, and Thuy Ai Huyen Le. "Evaluation of the HBV Genotype, Viral Load and Antivirus Drug Resistance Mutation in Tay Ninh Hospital, Vietnam by Real-Time PCR." In IFMBE Proceedings, 605–9. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-5859-3_103.

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Watson, Geoffrey Alan, Kirsty Taylor, and Lillian L. Siu. "Innovation and Advances in Precision Medicine in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 355–73. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_24.

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AbstractThe clinical utility of precision medicine through molecular characterization of tumors has been demonstrated in some malignancies, especially in cases where oncogenic driver alterations are identified. Next generation sequencing data from thousands of patients with head and neck cancers have provided vast amounts of information about the genomic landscape of this disease. Thus far, only a limited number of genomic alterations have been druggable, such as NTRK gene rearrangements in salivary gland cancers (mainly mammary analogue secretory carcinoma), NOTCH mutations in adenoid cystic cancers, HRAS mutations in head and neck squamous cell cancers, and even a smaller number of these have reached regulatory approval status. In order to expand the scope of precision medicine in head and neck cancer, additional evaluation beyond genomics is necessary. For instance, there is increasing interest to perform transcriptomic profiling for target identification. Another advance is in the area of functional testing such as small interfering RNA and drug libraries on patient derived cell cultures. Liquid biopsies to detect specific tumor clones or subclones, or viral sequences such as HPV, are of great interest to enable non-invasive tracking of response or resistance to treatment. In addition, precision immuno-oncology is a tangible goal, with a growing body of knowledge on the interactions between the host immunity, the tumor and its microenvironment. Immuno-oncology combinations that are tailored to immunophenotypes of the host-tumor-microenvironment triad, personalized cancer vaccines, and adoptive cell therapies, among others, are in active development. Many therapeutic possibilities and opportunities lie ahead that ultimately will increase the reality of precision medicine in head and neck cancer.
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Domingo, Esteban, Luis Menéndez-Arias, Miguel E. QuiñonesMateu, Africa Holguín, Mónica Gutiérrez-Rivas, Miguel A. Martínez, Josep Quer, Isabel S. Novella, and John J. Holland. "Viral quasispecies and the problem of vaccine-escape and drug-resistant mutants." In Progress in Drug Research/Fortschritte der Arzneimittelforschung/Progrès des recherches pharmaceutiques, 99–128. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-8861-5_4.

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Karlström, A. R., C. F. R. Källander, J. S. Gronowitz, and P. J. Wistrand. "Relevance of Viral Thymidine Kinase for Clinical Resistance to Antiviral Drugs When Treating Herpes Simplex Eye Infections." In Herpetic Eye Diseases, 187–92. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5518-9_26.

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Conference papers on the topic "Viral Drug Resistance"

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Zhang, Lei. "P3.132 Projecting the epidemiological effect, cost-effectiveness and transmission of hiv drug resistance in vietnam associated with viral load monitoring strategies." In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.367.

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Lobis, Yusuf Bachtiyar, Bhisma Murti, and Hanung Prasetya. "Influences of Peer Support Group and Psychosocio- Economic Determinants on Treatment Compliance in Hiv/Aids Patients in Sragen, Central Java." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.02.59.

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Background: Adherence to treatment is important to reduce viral replication, improve clinical and immunological conditions, reduce the risk of developing ARV resistance, and reduce the risk of HIV transmission. Peer support is suspected to be one of the factors driving drug intake adherence in patients with chronic disease. This study aimed to examine the influences of peer support and psychosocio-economic determinants on treatment compliance in HIV/AIDS patients. Subjects and Method: This was a case control design study conducted in Sragen, Central Java, Indonesia. A sample of 200 people with HIV/AIDS (PLWH) was selected by fixed disease sampling. The dependent variable was treatment compliance. The independent variables were knowledge toward HIV/AIDS, perceived benefit, perceived belief, perceived threat, perceived susceptibility, perceived seriousness, perceived barrier, attitude, indirect experience, family support, and peer support. The data were obtained from medical record and questionnaire. The data were analyzed by a multiple logistic regression run on Stata 13. Results: Treatment compliance increased with strong peer support (b= 1.34; 95% CI= 0.31 to 2.38; p= 0.011), strong family support (b= 1.09; 95% CI= 0.16 to 2.02; p= 0.021), knowledge toward HIV/AIDS (b= 1.65; 95% CI= 0.67 to 2.64; p= 0.001), high perceived benefit (b= 1.23; 95% CI= 0.28 to 2.18; p= 0.011), perceived belief (b= 2.05; 95% CI= 0.98 to 3.12; p<0.001), and high perceived threat (b= 1.22; 95% CI= 0.30 to 2.13; p= 0.009). Treatment compliance decreased with negative attitude (b= -2.47; 95% CI= -3.58 to -1.37; p <0.001), low perceived susceptibility (b= -1.26; 95% CI= -2.24 to – 0.27; p= 0.012), low perceived seriousness (b= -1.11; 95% CI= -2.06 to -0.16; p=0.021), high perceived barrier (b= -1.76; 95% CI= -2.81 to -0.70; p= 0.001), and indirect experience (b= -1.10; 95% CI= -2.05 to -0.14; p= 0.024). Conclusion: Treatment compliance increases with strong peer support, strong family support, high knowledge toward HIV/AIDS, high perceived benefit, perceived belief, and high perceived threat. Treatment compliances decrease with negative attitude, low perceived susceptibility, low perceived seriousness, high perceived barrier, and indirect experience. Keywords: HIV/AIDS, treatment compliance, peer support, psychosocial economy Correspondence: Yusuf Bachtiyar Lobis. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: bachtiyar03@gmail.com. Mobile: +628111388841. DOI: https://doi.org/10.26911/the7thicph.02.59
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Rabbani, Naila, Paul John Thornalley, Maryam Al-Motawa, and Mingzhan Xue. "Vulnerabilities of the SARS-Cov-2 Virus to Proteotoxicity – Opportunity for Repurposed Chemotherapy of COVID-19 Infection." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0291.

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The global pandemic of COVID-19 disease caused by infection with the SARS-CoV-2 Coronavirus, has produced an urgent requirement and search for improved treatments whilst effective vaccines are developed. A strategy for improved drug therapy is to increase levels of endogenous reactive metabolites for selective toxicity to SARS-CoV-2 by preferential damage to the viral proteome. Key reactive metabolites producing major quantitative damage to the proteome in physiological systems are: Reactive oxygen species (ROS) and the reactive glycating agent methylglyoxal (MG); cysteine residues and arginine residues are their most susceptible targets, respectively. From sequenced-based prediction of the SARS-CoV-2 proteome, we found 0.8-fold enrichment or depletion of cysteine residues in functional domains of the viral proteome; whereas there was a 4.6-fold enrichment of arginine residues, suggesting SARS-CoV-2 is resistant to oxidative agents and sensitive to MG. We examined activated arginine residues in functional domain with predicted low pKa by neighboring group interaction in the SARS-CoV-2. We found 25 such arginine residues, including 2 in the spike protein and 10 in the nucleoprotein. These sites were partially conserved in related coronaviridae: SARS-COV and MERS. We also screened and identified drugs, which increase cellular MG concentration to virucidal levels and found two antitumor drugs with historical antiviral activity, doxorubicin and paclitaxel were the best candidate for repurposing. Our findings provide evidence of potential vulnerability of SARS-CoV2 to inactivation by MG and a scientific rationale for repurposing of doxorubicin and paclitaxel for treatment of COVID-19 disease, providing efficacy and adequate therapeutic index may be established.
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Benslimane, Fatiha M., Hebah Al Khatib, Dana Albatesh, Ola Al-Jamal, Sonia Boughattas, Asmaa A. Althani, and Hadi M. Yassine. "Nanopore Sequencing SARS-CoV-2 Genome in Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0289.

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Background: The current pandemic, COVID-19, is cause by an RNA Coronavirus that was recently identified as SARS-CoV-2. RNA viruses tend to have a high mutation rate; the rate is around a million times greater than that of their hosts. The mutagenic potential of the virus depends on many factors, including the fidelity of nucleic acid-replicating viral enzymes, such as SARSCoV-2 RNA dependent RNA polymerase (RdRp). The rate of mutation drives viral evolution and genome variability, consequently allowing viruses to escape the immunity of the host and develop resistance to drugs. Therefore, the characterization of SARS-CoV-2 variants might lead to implement better therapeutics treatments, vaccines design and identify new diagnostics approaches. Aim: The aim of this study was to establish a fast sequencing method to identify SARS-CoV-2 mutations in Qatar. This will help to assess if there are new viral variants that are spreading in country. Methods: RNA was isolated from samples collected from Qatar COVID-19 positive patients. The Artic Network V3 primer scheme and Oxford Nanopore ligation sequencing kit were used to prepare the sequencing libraries. Libraries were loaded on to R9.4.1 flow cells and ran on a GridION. Bioinformatics analysis was done following the Artic Network SARA-CoV-2 bioinformatics tools. Results: Genome coverage of sequenced samples was >80% and the depth was average at 200x. The coverage was highly dependable on sample viral load; samples of CT value lower than 30 resulted in better sequence coverage. The sequenced genomes were deposited in GISAID and were mainly clustering with genomes deposited from the UK. Sequences were compared to Illumina and sanger sequences and they showed compatible results. Conclusion: The use of ONT to sequence SARA-CoV-2 is a quick, affordable, and reliable technique to determine viral mutation. Using this technique, the first sequences from Qatar were deposited in to GISAID. Up to date, 700 genomes have been sequenced from Qatari samples.
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Khudadad, Hanan, and Lukman Thalib. "Antibiotics Prescription Patterns in Primary Health Care in Qatar – A Population based study from 2017 to 2018." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0169.

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Background: Antibiotics are antimicrobial drugs used in the treatment and prevention of bacterial infections. They played a pivotal role in achieving major advances in medicine and surgery (1). Yet, due to increased and inappropriate use of antibiotics, antibiotic resistance (AR) has become a growing public health problem. Information on antibiotic prescription patterns are vital in developing a constructive approach to deal with growing antibiotic resistance (2). The study aims to describe the population based antibiotic prescriptions among patients attending primary care centers in Qatar. Methodology: A population based observational study of all medications prescribed in the all Primary Health Care Centers during the period of 2017-2018 in Qatar. Records with all medication prescriptions were extracted and linked to medical diagnosis. Antibiotics prescriptions records were compared to non- antibiotics records using logistic regression model in identifying the potential predictors for antibiotic prescriptions. Results: A total of 11,069,439 medication prescriptions given over a period of two-years, we found about 12.1% (n= 726,667) antibiotics prescriptions were antibiotics, and 65% of antibiotics are prescribed and received by the patients at the first visits. Paracetamol (22.3%) was the first highest medication prescribed followed by antibiotics (12.1 %) and vitamin D2 (10.2 %). More than half of all antibiotics prescribed during the period of January 2017 to December 2018 were Penicillin (56.9%). We found that half of the antibiotics (49.3 %) have been prescribed for the respiratory system comparing to the other body system. We found that males were 29% more likely be given an antibiotic compared to females (OR=1.29, 95% CI= 1.24- 1.33). Implications: The study provides a baseline data to enable PHCC management to design effective intervention program to address the problem of antibiotics resistance. Furthermore, it will help the policymakers to comprehend the size of the issue and develop a system to manage the antibiotics therapy. Conclusion: Antibiotics was the second highest medication prescribed in the Primary Health Care Centers in Qatar after paracetamol and most of the patients received it at the first visit. Most of the prescriptions in Primary Health Care Centers in Qatar were for the respiratory system, and Penicillin was the highest class prescribed. Male visitors were prescribed antibiotics more than female visitors.
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Maradey Lázaro, Jessica Gissella, Sergio Andrés Ardila Gómez, and Helio Sneyder Esteban Villegas. "Aerodynamics Analysis for Optimization the Design of a Baja SAE Chassis." In ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-88027.

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The aerodynamic analysis of vehicles using Computational Fluid Dynamics (CFD) is a powerful tool that is used to explore and investigate how air flow behaves around the vehicle, gives a qualitative idea of aerodynamic behavior and provides engineers with the information necessary to design the pieces that will be tested in the wind tunnel. This technique allows to find the values of forces and moments to get an idea of the drag resistance and lift forces on the vehicle. It is also possible to determine the position of the center of pressure that exerts a vital importance in the definition of the directional stability of the vehicle in its lateral dynamics. On the other hand, it offers the advantage of being able to see many variables of the problem that are very difficult to access in reality, for example to see current lines, vortex shedding, fields of pressures around the vehicle. Although the use of CFD has become a common practice in the automotive industry in recent decades, it is still not considered as a single technique, since one of the limitations is related to the dynamics of a turbulent flow is quite complex so which analytical and computational study depends on what is called Turbulence Models. This article aims to show the aerodynamic design process by CFD simulation of a Baja SAE vehicle chassis using Ansys software, widely used for simulation of static charges, thermodynamics, fluid mechanics, multiphysics systems and vibrations and to provide information that can be validated experimentally in the future.
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