ArticleAntimicrobial agents and chemotherapy2013
Impact of primary elvitegravir resistance-associated mutations in HIV-1 integrase on drug susceptibility and viral replication fitness.
Article in Antimicrobial agents and chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed.
- Predicting the evolutionary and structural compensation in Tat ARM region across HIV-1 groups using machine learning approach.Scientific reports · 2026Article
- Low Prevalence of Integrase Inhibitor Resistance Following Treatment Failure: A Real-World Analysis from Hunan Province, China.Infection and drug resistance · 2026Article
- Elucidating the mechanism by which HIV-1 nucleocapsid mutations confer resistance to integrase strand transfer inhibitors.Science advances · 2025Article
- Elucidating the Mechanism by Which HIV-1 Nucleocapsid Mutations Confer Resistance to Integrase Strand Transfer Inhibitors.bioRxiv : the preprint server for biology · 2025Article
- Frequency of Major Transmitted Integrase Resistance in Poland Remains Low Despite Change in Subtype Variability.Viruses · 2024Article
- Decoupling HIV-1 antiretroviral drug inhibition from plasma antibody activity to evaluate broadly neutralizing antibody therapeutics and vaccines.Cell reports. Medicine · 2024Article
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- Prevalence of HIV-1 Natural Polymorphisms and Integrase-Resistance-Associated Mutations in African Children.Viruses · 2023Article
- Effectiveness and safety of integrase strand transfer inhibitors in Spain: a prospective real-world study.Frontiers in cellular and infection microbiology · 2023Article
- Drug Resistance to Integrase Strand-Transfer Inhibitors among HIV-1-Infected Adults in Guangdong, China.Pathogens (Basel, Switzerland) · 2022Article
- 2022 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2022Article
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- Interaction analysis of statistically enriched mutations identified in Cameroon recombinant subtype CRF02_AG that can influence the development of Dolutegravir drug resistance mutations.BMC infectious diseases · 2021Article
- Short Communication: Integrase Strand Transfer Inhibitors Drug Resistance Mutations in Puerto Rico HIV-Positive Individuals.International journal of environmental research and public health · 2021Article
- Pretreatment HIV drug resistance spread within transmission clusters in Mexico City.The Journal of antimicrobial chemotherapy · 2020Article
- Variability in HIV-1 Integrase Gene and 3'-Polypurine Tract Sequences in Cameroon Clinical Isolates, and Implications for Integrase Inhibitors Efficacy.International journal of molecular sciences · 2020Article
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- 2019 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2019Article
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14 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Elvitegravir (EVG) is an effective HIV-1 integrase (IN) strand transfer inhibitor (INSTI) in advanced clinical development. Primary INSTI resistance-associated mutations (RAMs) at six IN positions have been identified in HIV-1-infected patients failing EVG-containing regimens in clinical studies: T66I/A/K, E92Q/G, T97A, S147G, Q148R/H/K, and N155H. In this study, the effect of these primary IN mutations, alone and in combination, on susceptibility to the INSTIs EVG, raltegravir (RAL), and dolutegravir (DTG); IN enzyme activities; and viral replication fitness was characterized. Recombinant viruses containing the six most common mutations exhibited a range of reduced EVG susceptibility: 92-fold for Q148R, 30-fold for N155H, 26-fold for E92Q, 10-fold for T66I, 4-fold for S147G, and 2-fold for T97A. Less commonly observed primary IN mutations also showed a range of reduced EVG susceptibilities: 40- to 94-fold for T66K and Q148K and 5- to 10-fold for T66A, E92G, and Q148H. Some primary IN mutations exhibited broad cross-resistance between EVG and RAL (T66K, E92Q, Q148R/H/K, and N155H), while others retained susceptibility to RAL (T66I/A, E92G, T97A, and S147G). Dual combinations of primary IN mutations further reduced INSTI susceptibility, replication capacity, and viral fitness relative to either mutation alone. Susceptibility to DTG was retained by single primary IN mutations but reduced by dual mutation combinations with Q148R. Primary EVG RAMs also diminished IN enzymatic activities, concordant with their structural proximity to the active site. Greater reductions in viral fitness of dual mutation combinations may explain why some primary INSTI RAMs do not readily coexist on the same HIV-1 genome but rather establish independent pathways of resistance to EVG.
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