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Journal articles on the topic 'HIV Drug Resistance'

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Published: 4 June 2021
Last updated: 21 February 2023

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1

Clavel, François, and Allan J. Hance. "HIV Drug Resistance." New England Journal of Medicine 350, no. 10 (March 4, 2004): 1023–35. http://dx.doi.org/10.1056/nejmra025195.

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2

Richman, D. D. "HIV Drug Resistance." Annual Review of Pharmacology and Toxicology 33, no. 1 (April 1993): 149–64. http://dx.doi.org/10.1146/annurev.pa.33.040193.001053.

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3

RICHMAN, DOUGLAS D. "HIV Drug Resistance." AIDS Research and Human Retroviruses 8, no. 6 (June 1992): 1065–71. http://dx.doi.org/10.1089/aid.1992.8.1065.

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4

Schmit, Jean-Claude. "HIV drug resistance." HIV Clinical Trials 3, no. 3 (May 2002): 225–26. http://dx.doi.org/10.1310/kmkn-ke48-2gwu-g0he.

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5

Calmy, Alexandra, Fernando Pascual, and Nathan Ford. "HIV Drug Resistance." New England Journal of Medicine 350, no. 26 (June 24, 2004): 2720–21. http://dx.doi.org/10.1056/nejm200406243502621.

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6

Richman, Douglas D. "HIV DRUG RESISTANCE." AIDS 8, Supplement 4 (November 1994): S3. http://dx.doi.org/10.1097/00002030-199411004-00010.

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7

Nadia, Rizka, Dwitya Elvira, and Raveinal. "HIV Drug Resistance Mutations." Bioscientia Medicina : Journal of Biomedicine and Translational Research 6, no. 7 (May 27, 2022): 2006–13. http://dx.doi.org/10.37275/bsm.v6i7.547.

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ART resistance, according to WHO, is the presence of one or more mutations in HIV that reduces the ability of certain drugs or drug groups to inhibit viral replication. According to the 2019 HIV Drug Resistance Report issued by the WHO, the prevalence of Antiretroviral Therapy (ART) drug resistance is 3%-29%. The prevalence of HIV drug resistance varies by country. In developed countries, the prevalence ranges from 6.6% to 11%. There are two types of resistance to ART: primary and secondary resistance. Primary resistance reflects the acquisition of drug-resistant strains in individuals who have recently been infected and have not received therapy. Secondary resistance occurs after treatment with ART. Resistance to antiretroviral therapy, mainly NRTIs, NNRTIs, and protease inhibitors, is caused by continuous inhibition of the HIV reverse transcriptase enzyme. World Health Organization (WHO) has recommended two NRTIs plus Lopinavir or Atazanavir as a second-line regimen for individuals who have failed treatment with efavirenz or dolutegravir; two NRTIs plus Darunavir and Lopinavir plus Raltegravir are recommended as an alternative due to cost constraints and the fact that Darunavir is unstable in moderately hot conditions.
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8

Salvana, Edsel Maurice, Brian Schwem, Christine Penalosa, Geraldine Arevalo, Nina Dungca, Jodor Lim, Katerina Leyritana, and Raul Destura. "HIV Transmitted Drug Resistance in the Philippines: The Case for Baseline Genotyping and Drug Resistance Testing." Open Forum Infectious Diseases 4, suppl_1 (2017): S423. http://dx.doi.org/10.1093/ofid/ofx163.1064.

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Abstract Background The Philippines has one of the fastest growing HIV epidemics in the world. Parallel to the increase is a shift in HIV subtype from B to CRF01_AE. No transmitted drug resistance (TDR) surveillance has ever been conducted. With the widespread rollout of antiretrovirals and the limited repertoire of 6 drugs (tenofovir, lamivudine, zidovudine, nevirapine, efavirenz, lopinavir/ritonavir) makes TDR monitoring imperative. In addition, a high rate of hepatitis B (HBV) co-infection (17%) in the general population raises the risk of TDR with prior NRTI monotherapy. Methods Following IRB approval, we performed TDR surveillance at the Philippine General Hospital, one of the largest tertiary referral centers in the country. Treatment-naïve patients had their HIV RT and PR genes sequenced using WHO approved-protocols for HIV genotyping. Generated sequences were analyzed using the Stanford Drug Resistance Database. Pertinent demographic and clinical data were collected. The current results represent year 1 of the study. Results 95 treatment naïve patients were analyzed. Median age was 30 years (range 20–68). There were 88 males and 7 females. Median CD4 count was 90 cells/mL (range 0–936) and median viral load was 1792000 copies/mL. 18 patients were co-infected with HBV, but all denied previous HBV treatment. Conclusion The TDR rate for HIV in the Philippines is 6.3%. This is above the threshold for recommending baseline TDR genotyping for all local HIV patients. All HIV with TDR were subtype CRF01_AE, and this may signal a higher risk of TDR as the epidemic shifts further to a non-B subtype. Disclosures E. M. Salvana, Merck: Scientific Advisor and Speaker’s Bureau, Consulting fee and Speaker honorarium
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9

Tilghman, MW, J. Pérez-Santiago, G. Osorio, SJ Little, DD Richman, WC Mathews, RH Haubrich, and DM Smith. "Community HIV-1 drug resistance is associated with transmitted drug resistance." HIV Medicine 15, no. 6 (January 12, 2014): 339–46. http://dx.doi.org/10.1111/hiv.12122.

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10

Lazzari, Stefano, Annapaola de Felici, Howard Sobel, and Silvia Bertagnolio. "HIV Drug Resistance Surveillance." AIDS 18, Supplement 3 (June 2004): S49—S53. http://dx.doi.org/10.1097/00002030-200406003-00010.

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11

Mascolini, Mark, Charles Boucher, Brendan Larder, John Mellors, and Douglas Richman. "Key Reports from the XV International HIV Drug Resistance Workshop 2006." Antiviral Therapy 12, no. 1 (January 2007): 131–46. http://dx.doi.org/10.1177/135965350701200118.

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The XV International HIV Drug Resistance Workshop recorded advances in basic and clinical science of HIV resistance to antiretrovirals as well as new findings on resistance by hepatitis B virus (HBV) and hepatitis C virus (HCV). In the clinical arena, attendees learned of four cases of resistance to lopinavir/ritonavir monotherapy, correlation between low-frequency pretreatment mutations and failure of a first antiretroviral regimen, emergence of non-nucleoside-related mutations in 20% of patients interrupting a suppressive nonnucleoside regimen, and evolution of mutations conferring resistance to an HIV entry inhibitor that is being studied as a vaginal microbicide. New data reported from the POWER 1, 2 and 3 salvage trials suggested that there is a close correlation between darunavir (TMC114) phenotypic susceptibility, the number of baseline protease inhibitor-related resistance mutations and virological response. Scientists exploring the mechanisms of resistance reported of mutations in the carboxy-terminal domain of reverse transcriptase that may further resistance to zidovudine, novel mutations that may contribute to resistance of both nucleoside and non-nucleoside reverse transcriptase inhibitors, and a mechanism that HCV and HIV may share to resist antiviral therapy.
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12

Pennings, Pleuni S. "HIV drug resistance: problems and perspectives." Infectious Disease Reports 5, no. 1S (June 6, 2013): 5. http://dx.doi.org/10.4081/idr.2013.s1.e5.

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Access to combination antiretroviral treatment (ART) has improved greatly over recent years. At the end of 2011, more than eight million HIV-infected people were receiving ART in low-income and middle-income countries. ART generally works well in keeping the virus suppressed and the patient healthy. However, treatment only works as long as the virus is not resistant against the drugs used. In the last decades, HIV treatments have become better and better at slowing down the evolution of drug resistance, so that some patients are treated for many years without having any resistance problems. However, for some patients, especially in low-income countries, drug resistance is still a serious threat to their health. This essay will review what is known about transmitted and acquired drug resistance, multi-class drug resistance, resistance to newer drugs, resistance due to treatment for the prevention of mother-to-child transmission, the role of minority variants (low-frequency drug-resistance mutations), and resistance due to pre-exposure prophylaxis.
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13

Sönnerborg, Anders. "8th European HIV Drug Resistance Workshop." HIV Therapy 4, no. 3 (May 2010): 285–87. http://dx.doi.org/10.2217/hiv.10.22.

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14

Shafer, Robert W. "Genotypic Testing for Human Immunodeficiency Virus Type 1 Drug Resistance." Clinical Microbiology Reviews 15, no. 2 (April 2002): 247–77. http://dx.doi.org/10.1128/cmr.15.2.247-277.2002.

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SUMMARY There are 16 approved human immunodeficiency virus type 1 (HIV-1) drugs belonging to three mechanistic classes: protease inhibitors, nucleoside and nucleotide reverse transcriptase (RT) inhibitors, and nonnucleoside RT inhibitors. HIV-1 resistance to these drugs is caused by mutations in the protease and RT enzymes, the molecular targets of these drugs. Drug resistance mutations arise most often in treated individuals, resulting from selective drug pressure in the presence of incompletely suppressed virus replication. HIV-1 isolates with drug resistance mutations, however, may also be transmitted to newly infected individuals. Three expert panels have recommended that HIV-1 protease and RT susceptibility testing should be used to help select HIV drug therapy. Although genotypic testing is more complex than typical antimicrobial susceptibility tests, there is a rich literature supporting the prognostic value of HIV-1 protease and RT mutations. This review describes the genetic mechanisms of HIV-1 drug resistance and summarizes published data linking individual RT and protease mutations to in vitro and in vivo resistance to the currently available HIV drugs.
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15

Kuritzkes, Daniel R. "Recent developments in HIV-1 drug resistance." Drug Resistance Updates 2, no. 2 (April 1999): 127–29. http://dx.doi.org/10.1054/drup.1999.0079.

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16

Clutter, Dana S., Michael R. Jordan, Silvia Bertagnolio, and Robert W. Shafer. "HIV-1 drug resistance and resistance testing." Infection, Genetics and Evolution 46 (December 2016): 292–307. http://dx.doi.org/10.1016/j.meegid.2016.08.031.

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17

Baldwin, Chris, and Ben Berkhout. "HIV-1 drug-resistance and drug-dependence." Retrovirology 4, no. 1 (2007): 78. http://dx.doi.org/10.1186/1742-4690-4-78.

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18

Chaix-Couturier, Carine, Christopher Holtzer, Kathryn A. Phillips, Isabelle Durand-Zaleski, and John Stansell. "HIV-1 Drug Resistance Genotyping." PharmacoEconomics 18, no. 5 (November 2000): 425–33. http://dx.doi.org/10.2165/00019053-200018050-00002.

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19

Moreno, Milagros, Estrella Caballero, Raquel M. Mateus, Filomena Samba, Eva Gil, and Vicenç Falcó. "HIV drug resistance in Africa." AIDS 31, no. 11 (July 2017): 1637–39. http://dx.doi.org/10.1097/qad.0000000000001536.

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20

Balter, M. "AIDS RESEARCH:Outsmarting HIV Drug Resistance." Science 282, no. 5394 (November 27, 1998): 1623b—1623. http://dx.doi.org/10.1126/science.282.5394.1623b.

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21

Frenkel, Lisa M., and Nicole H. Tobin. "Understanding HIV-1 Drug Resistance." Therapeutic Drug Monitoring 26, no. 2 (April 2004): 116–21. http://dx.doi.org/10.1097/00007691-200404000-00005.

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22

De Felici, Annapaola. "Global HIV drug resistance surveillance." Scandinavian Journal of Infectious Diseases 35, no. 11 (December 2003): 21–23. http://dx.doi.org/10.1080/03008870310009605.

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23

Sethi, Ajay K. "Adherence and HIV Drug Resistance." HIV Clinical Trials 5, no. 2 (April 2004): 112–15. http://dx.doi.org/10.1310/n53e-1930-njmw-gl7c.

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24

BORMAN, STU. "ANTI-HIV DRUG SIDESTEPS RESISTANCE." Chemical & Engineering News 86, no. 6 (February 11, 2008): 14. http://dx.doi.org/10.1021/cen-v086n006.p014.

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25

Kuritzkes, Daniel R. "Drug resistance in HIV-1." Current Opinion in Virology 1, no. 6 (December 2011): 582–89. http://dx.doi.org/10.1016/j.coviro.2011.10.020.

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26

Geretti, Anna Maria, Roger Paredes, and Michael J. Kozal. "Transmission of HIV drug resistance." Current Opinion in Infectious Diseases 28, no. 1 (February 2015): 23–30. http://dx.doi.org/10.1097/qco.0000000000000136.

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27

Grezina, L. A., N. E. Dement'eva, N. N. Zajtseva, E. V. Kazennova, D. E. Kireev, and A. B. Shemshura. "Analysis of HIV drug resistance." Laboratornaya sluzhba 6, no. 3 (2017): 217. http://dx.doi.org/10.17116/labs201763217-237.

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28

Davenport;, M. P. "Reversibility of HIV Drug Resistance." Science 288, no. 5470 (May 26, 2000): 1299a—1299. http://dx.doi.org/10.1126/science.288.5470.1299a.

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29

Godfrey, Catherine, Michael C. Thigpen, Keith W. Crawford, Patrick Jean-Phillippe, Deenan Pillay, Deborah Persaud, Daniel R. Kuritzkes, Mark Wainberg, Elliot Raizes, and Joseph Fitzgibbon. "Global HIV Antiretroviral Drug Resistance." Journal of Infectious Diseases 216, suppl_9 (June 17, 2017): S798—S800. http://dx.doi.org/10.1093/infdis/jix137.

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30

Mulwa, Lucky, and Marc Stadler. "Antiviral Compounds from Myxobacteria." Microorganisms 6, no. 3 (July 19, 2018): 73. http://dx.doi.org/10.3390/microorganisms6030073.

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Viral infections including human immunodeficiency virus (HIV), cytomegalovirus (CMV), hepatitis B virus (HBV), and hepatitis C virus (HCV) pose an ongoing threat to human health due to the lack of effective therapeutic agents. The re-emergence of old viral diseases such as the recent Ebola outbreaks in West Africa represents a global public health issue. Drug resistance and toxicity to target cells are the major challenges for the current antiviral agents. Therefore, there is a need for identifying agents with novel modes of action and improved efficacy. Viral-based illnesses are further aggravated by co-infections, such as an HIV patient co-infected with HBV or HCV. The drugs used to treat or manage HIV tend to increase the pathogenesis of HBV and HCV. Hence, novel antiviral drug candidates should ideally have broad-spectrum activity and no negative drug-drug interactions. Myxobacteria are in the focus of this review since they produce numerous structurally and functionally unique bioactive compounds, which have only recently been screened for antiviral effects. This research has already led to some interesting findings, including the discovery of several candidate compounds with broad-spectrum antiviral activity. The present review looks at myxobacteria-derived antiviral secondary metabolites.
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31

Parczewski, Miłosz. "Drug resistance among patients with HIV-1." Forum Zakażeń 4, no. 5 (December 4, 2013): 317–23. http://dx.doi.org/10.15374/fz2013054.

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32

Sharma, Roopali. "Antiretroviral Resistance: Mechanisms, Detection and Clinical Implications." Journal of Pharmacy Practice 13, no. 6 (December 2000): 442–56. http://dx.doi.org/10.1106/hl1t-9yme-kmf1-nynv.

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Widespread use of antiretroviral agents and the epidemic of human immunodeficiency virus (HIV) strains resistant to these drugs have raised a lot of issues including the biology and clinical implications of HIV resistance, reliability of resistant assays and their role in clinical practice. In May 2000, the International AIDS panel endorsed and recommended the use of antiretroviral drug resistance testing in patients. Considerable data on HIV drug resistance testing that strongly suggest that utility of these assays may be of great value have been published and presented at major meetings. Although the genotypic and phenotypic assays are available for antiretroviral drug resistance testing, the testing has certain limitations. The role of these resistance assays is not clearly defined in clinical practice. Prospective studies are needed to define the long-term benefits of these assays. HIV drug resistance testing in the near future may become an important tool and standard of practice for patients infected with HIV. Clinicians caring for HIV-positive patients should be familiar with the antiretroviral drug resistant assays.
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33

T. Weber, Irene, and Robert W. Harrison. "Tackling the problem of HIV drug resistance." Postępy Biochemii 62, no. 3 (November 18, 2016): 273–79. http://dx.doi.org/10.18388/pb.2016_26.

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The virally-encoded HIV-1 protease is an effective target for antiviral drugs, however, treatment for HIV infections is limited by the prevalence of drug resistant viral mutants. In this review, we describe our three-pronged approach to analyze and combat drug resistance. Understanding the molecular basis for resistance due to protease inhibitors is a key initial step in this approach. This knowledge is being employed for the design of new, improved inhibitors with high affinity for resistant mutants as well as wild type enzyme. In parallel with experimental studies of diverse mutants and inhibitory compounds, we are developing efficient algorithms to predict drug resistance phenotype from genotype data. This approach has important practical applications in the clinic where genotyping is recommended for individuals with new infections.
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34

Ostankova, Yu V., D. E. Valutite, E. B. Zueva, E. N. Serikova, A. N. Shchemelev, S. Boumbaly, T. A. L. Balde, and A. V. Semenov. "Primary HCV Drug Resistance Mutations in Patients with Newly Diagnosed HIV Infection." Problems of Particularly Dangerous Infections, no. 3 (October 22, 2020): 97–105. http://dx.doi.org/10.21055/0370-1069-2020-3-97-105.

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Objective of our work was to assess prevalence of the primary HCV drug resistance mutations in the NS5b gene in patients with newly diagnosed HIV infection.Materials and methods. The study material was 196 blood plasma samples from patients living in the North-Western Federal District with newly diagnosed HIV. Samples were examined for the anti-HCV antibodies and HCV RNA presence. If HCV RNA was detected, amplification was performed using three primers pairs that co-flanked the NS5b gene. After sequencing the indicated gene nucleotide sequence, the virus subtype was determined and drug resistance mutations were detected.Results and discussion. Antibodies to HCV were detected in 18.87 % of HIV-infected individuals. HCV RNA was detected in 18.36 % of the patients, including 89.18 % anti-HCV-positive and 1.88 % anti-HCV-negative. It was shown that co-infection is more common in men (77.8 %) compared to women (22.2 %) – χ2 = 3.996 at p = 0.0456, df = 2. The difference in the HIV viral load between the groups with HIV monoinfection and with HIV + HCV coinfection was demonstrated (χ2 = 6.284 at p = 0.0432, df = 2). A significant difference between the groups by the CD4 + lyphocytes number was shown. In the phylogenetic analysis, the HCV subtypes are distributed as follows: HCV 1b – 47.2 %, HCV 3a – 30.6 %, HCV 1a – 13.9 %, HCV 2a – 5.5 % and only one sample was defined as HCV 2k – 2.8 %, respectively. Nine samples (25 %) presented NS5b mutations in the positions related to the development of drug resistance of HCV, including two samples among HCV genotypes 1a and 3a (i.e., 5.6 % of the total HIV + HCV group), as well as five samples among HCV 1b (13.9 % of the total group). Mutations among HCV 1a were C316Y and N444D substitutions. Among HCV 1b, C316N, C451S, S556N/G substitutions were identified. Among patients with HCV 3a, 2 samples (5.6 %) with a D310N mutation associated with an unfavorable disease prognosis were found. The introduction of direct sequencing of HCV nucleotide sequences into the routine laboratory diagnostics will allow us to estimate the primary drug resistance mutations prevalence in risk groups to predict the HCV life-threatening complications development – fibrosis, cirrhosis, hepatocellular carcinoma, as well as the outcome of antiviral therapy prognosis. The data obtained can be rationally used to assess the dynamics of the HCV primary pharmacoresistance prevalence among HIV-infected individuals.
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35

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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36

Yerly, Sabine, Stéphanie Jost, Amalio Telenti, Markus Flepp, Laurent Kaiser, Jean-Philippe Chave, Pietro Vernazza, et al. "Infrequent Transmission of HIV-1 Drug-Resistant Variants." Antiviral Therapy 9, no. 3 (April 1, 2003): 375–84. http://dx.doi.org/10.1177/135965350400900312.

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Transmission of drug-resistant variants is influenced by several factors, including the prevalence of drug resistance in the population of HIV-1-infected patients, HIV-1 RNA levels and transmission by recently infected patients. In order to evaluate the impact of these factors on the transmission of drug-resistant variants, we have defined the population of potential transmitters and compared their resistance profiles to those of newly infected patients. Sequencing of pol gene was performed in 220 recently infected patients and in 373 chronically infected patients with HIV-1 RNA >1000 copies/ml. Minimal and maximal drug-resistance profiles of potential transmitters were estimated by weighting resistance profiles of chronically infected patients with estimates of the Swiss HIV-1-infected population, the prevalence of exposure to antiviral drugs and the proportion of infections attributed to primary HIV infections. The drug-resistance prevalence in recently infected patients was 10.5% (one class drug resistance: 9.1%; two classes: 1.4%; three classes: 0%). Phylogenetic analysis revealed significant clustering for 30% of recent infections. The drug-resistance prevalence in chronically infected patients was 72.4% (one class: 29%; two classes: 27.6%; three classes: 15.8%). After adjustment, the risk of transmission relative to wild-type was reduced both for one class drug resistance (minimal and maximal estimates: odds ratio: 0.39, P<0.001; and odds ratio: 0.55, P=0.011, respectively), and for two to three class drug resistance (odds ratios: 0.05 and 0.07, respectively, P<0.001). Neither sexual behaviour nor HIV-1 RNA levels explained the low transmission of drug-resistant variants. These data suggest that drug-resistant variants and in particular multidrug-resistant variants have a substantially reduced transmission capacity.
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37

Kirichenko, A. A., D. E. Kireev, A. E. Lopatukhin, A. V. Murzakova, I. A. Lapovok, N. N. Ladnaya, and V. V. Pokrovsky. "PREVALENCE AND STRUCTURE OF HIV-1 DRUG RESISTANCE AMONG TREATMENT NAÏVE PATIENTS SINCE THE INTRODUCTION OF ANTIRETROVIRAL THERAPY IN THE RUSSIAN FEDERATION." HIV Infection and Immunosuppressive Disorders 11, no. 2 (July 2, 2019): 75–83. http://dx.doi.org/10.22328/2077-9828-2019-11-2-75-83.

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Aim: to analyze the prevalence, structure of drug resistance and drug resistance mutations in the protease and reverse transcriptase genes of HIV-1 among treatment naïve patients.Materials and methods. We analyzed protease and reverse transcriptase sequences from 1560 treatment naïve HIV-infected patients from all Federal Districts of the Russian Federation with the first positive immune blot during 1998–2017. Sequences were analyzed for the presence of drug resistance mutations and predicted drug resistance to antiretroviral drugs using two algorithms — Stanford HIVDR Database (HIVdb) and the 2009 SDRM list (CPR).Results. The prevalence of drug resistance mutations was 11,1%. More often the prevalence of drug resistance was found for non-nucleoside reverse transcriptase inhibitor drugs (rilpivirine, nevirapine, efavirenz). The prevalence of transmitted drug resistance associated with mutations from the SDRM list was 5,3%, which is classified by the WHO as a moderate level. However, it should be noted that since the large-scale use of antiretroviral drugs in the Russian Federation, there has been a trend towards a gradual increase in the level of the transmitted drug resistance, and in 2016 it has already reached 6,1%.Conclusion. The results demonstrate the need for regular surveillance of the prevalence of HIV drug resistance to antiretroviral drugs among treatment naïve patients in the Russian Federation.
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38

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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39

Bussmann, Hermann, Vladimir Novitsky, William Wester, Trevor Peter, Kereng Masupu, Lesego Gabaitiri, Soyeon Kim, et al. "HIV-1 Subtype C Drug-Resistance Background among ARV-Naive Adults in Botswana." Antiviral Chemistry and Chemotherapy 16, no. 2 (April 2005): 103–15. http://dx.doi.org/10.1177/095632020501600203.

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Current HIV-1 antiretroviral (ARV) drug resistance knowledge is limited to HIV-1 subtype B (HIV-1B). We addressed whether unique genetic and phenotypic properties of HIV-1 subtype C (HIV-1C), southern Africa's most prevalent subtype, may foment earlier and/or distinct resistance mutations. Population-level HIV-1C genotypes were evaluated with respect to drug resistance prevalence before Botswana's public ARV treatment programme began. Viruses were genotyped from 11 representative districts of northern and southern Botswana, and consensus sequences from these 71 individuals and 51 previously reported sequences from HIV-positive blood donors were constructed. Phylogenetic analysis classified all 71 sequences but one, which exhibited pol gene mosaicism, as HIV-1C. The protease and reverse transcriptase coding region had no detectable known primary mutations associated with HIV-1B protease inhibitor (PI) drug resistance. Secondary mutations associated with PI drug resistance were found in all sequences. Several HIV-1C—specific polymorphic sites were found across the pol gene. Northern and southern Botswana viral sequences showed no significant differences from each other. Population genotyping shows that, without countrywide ARV treatment, HIV-1C—infected Batswana harbour virtually no primary mutations known to confer resistance to the three major HIV-1B ARV drug classes. Some secondary PI mutations and polymorphic sites in the protease enzyme necessitate continuous population monitoring, particularly after introduction of countrywide ARV treatment in Botswana. Although its PI resistance development rate and kinetics are not known, our data may suggest increased susceptibility and readiness of HIV-1C to develop resistance under drug pressure when the PI class of drugs is used.
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John, Mina, Corey B. Moore, Ian R. James, and Simon A. Mallal. "Interactive Selective Pressures of Hla-Restricted Immune Responses and Antiretroviral Drugs on HIV-1." Antiviral Therapy 10, no. 4 (May 2005): 551–55. http://dx.doi.org/10.1177/135965350501000409.

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HIV-specific cytotoxic T lymphocyte (CTL) responses mediated by human leukocyte antigen (HLA) recognition and antiretroviral drugs exert selection pressure on HIV-1 in vivo. The selection of CTL escape mutations strongly underpins the failure of CTL control in most untreated infections whilst drug-resistance mutations predict failure of drug control. These two evolutionary forces share common target residues in HIV-1 at which their selection effects could be synergistic or antagonistic, such that the propensity to develop drug resistance and virological treatment failure may be influenced by HLA type. We examined HIV-1 reverse transcriptase (RT) and protease sequences in a large clinical observational cohort of 487 HIV-infected individuals and found evidence of site-specific interactions between specific antiretroviral drug exposures, HLA alleles and HIV sequence diversity at population level. Such interactions may have general and specific implications for explaining in vivo/in vitro discordance of drug resistance, host-specific susceptibility to drug resistance, individualization of therapy and therapeutic vaccine design.
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HANNA, GEORGE J., and ANGELA M. CALIENDO. "Testing for HIV-1 Drug Resistance." Molecular Diagnosis 6, no. 4 (2001): 253–63. http://dx.doi.org/10.2165/00066982-200106040-00007.

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Kolupajeva, Tatjana, Pauls Aldins, Ludmila Guseva, Diana Dusacka, Valentina Sondore, Ludmila Viksna, and Baiba Rozentale. "HIV Drug Resistance Tendencies in Latvia." Central European Journal of Public Health 16, no. 3 (September 1, 2008): 138–40. http://dx.doi.org/10.21101/cejph.a3473.

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43

Zdanowicz, Martin M. "The Pharmacology of HIV Drug Resistance." American Journal of Pharmaceutical Education 70, no. 5 (September 2006): 100. http://dx.doi.org/10.5688/aj7005100.

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44

Erickson, J. W., and S. K. Burt. "Structural Mechanisms of HIV Drug Resistance." Annual Review of Pharmacology and Toxicology 36, no. 1 (April 1996): 545–71. http://dx.doi.org/10.1146/annurev.pa.36.040196.002553.

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45

Cambiano, Valentina, Silvia Bertagnolio, Michael R. Jordan, Deenan Pillay, Joseph H. Perriëns, Francois Venter, Jens Lundgren, and Andrew Phillips. "Predicted levels of HIV drug resistance." AIDS 28 (January 2014): S15—S23. http://dx.doi.org/10.1097/qad.0000000000000082.

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46

Santos, André F., and Marcelo A. Soares. "HIV Genetic Diversity and Drug Resistance." Viruses 2, no. 2 (February 2, 2010): 503–31. http://dx.doi.org/10.3390/v2020503.

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Cortez, Karoll J., and Frank Maldarelli. "Clinical Management of HIV Drug Resistance." Viruses 3, no. 4 (April 14, 2011): 347–78. http://dx.doi.org/10.3390/v3040347.

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48

Check, Erika. "HIV drug resistance triggers strategic switch." Nature 424, no. 6947 (July 2003): 361. http://dx.doi.org/10.1038/424361a.

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Smith, Davey M., Joseph K. Wong, George K. Hightower, Caroline C. Ignacio, Kersten K. Koelsch, Christos J. Petropoulos, Douglas D. Richman, and Susan J. Little. "HIV drug resistance acquired through superinfection." AIDS 19, no. 12 (August 2005): 1251–56. http://dx.doi.org/10.1097/01.aids.0000180095.12276.ac.

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Stat, Terri Yablonsky. "HIV Drug Resistance on the Rise." Laboratory Medicine 30, no. 12 (December 1, 1999): 764–65. http://dx.doi.org/10.1093/labmed/30.12.764.

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