ArticleJournal of virology2000
High-level resistance to 3'-azido-3'-deoxythimidine due to a deletion in the reverse transcriptase gene of human immunodeficiency virus type 1.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- The effects of cryopreservation on PBMCs transcriptome profile.Frontiers in immunology · 2025Article
- A Triazinone Derivative Inhibits HIV-1 Replication by Interfering with Reverse Transcriptase Activity.ChemMedChem · 2016Article
- ASK1 restores the antiviral activity of APOBEC3G by disrupting HIV-1 Vif-mediated counteraction.Nature communications · 2015Article
- Significantly improved HIV inhibitor efficacy prediction employing proteochemometric models generated from antivirogram data.PLoS computational biology · 2013Article
- Thymidine analogue excision and discrimination modulated by mutational complexes including single amino acid deletions of Asp-67 or Thr-69 in HIV-1 reverse transcriptase.The Journal of biological chemistry · 2011Article
- Selection and characterization of HIV-1 with a novel S68 deletion in reverse transcriptase.Antimicrobial agents and chemotherapy · 2011Article
- Economic evaluation of ART in resource-limited countries.Current opinion in HIV and AIDS · 2010Review
- Clinical and genotypic findings in HIV-infected patients with the K65R mutation failing first-line antiretroviral therapy in Nigeria.Journal of acquired immune deficiency syndromes (1999) · 2009Article
- Phylogenetic and genetic analysis of feline immunodeficiency virus gag, pol, and env genes from domestic cats undergoing nucleoside reverse transcriptase inhibitor treatment or treatment-naïve cats in Rio de Janeiro, Brazil.Journal of virology · 2008Article
- Relative fitness and replication capacity of a multinucleoside analogue-resistant clinical human immunodeficiency virus type 1 isolate with a deletion of codon 69 in the reverse transcriptase coding region.Journal of virology · 2007Article
- Insertions in the human immunodeficiency virus type 1 protease and reverse transcriptase genes: clinical impact and molecular mechanisms.Antimicrobial agents and chemotherapy · 2005Review
- Effects of the Delta67 complex of mutations in human immunodeficiency virus type 1 reverse transcriptase on nucleoside analog excision.Journal of virology · 2004Article
- Actinomycin D induces high-level resistance to thymidine analogs in replication of human immunodeficiency virus type 1 by interfering with host cell thymidine kinase expression.Journal of virology · 2003Article
- Genotypic testing for human immunodeficiency virus type 1 drug resistance.Clinical microbiology reviews · 2002Review
- Augmentation of human immunodeficiency virus type 1 subtype E (CRF01_AE) multiple-drug resistance by insertion of a foreign 11-amino-acid fragment into the reverse transcriptase.Journal of virology · 2001Article
- Amino acid deletion at codon 67 and Thr-to-Gly change at codon 69 of human immunodeficiency virus type 1 reverse transcriptase confer novel drug resistance profiles.Journal of virology · 2001Article
- Relative replication fitness of a high-level 3'-azido-3'-deoxythymidine-resistant variant of human immunodeficiency virus type 1 possessing an amino acid deletion at codon 67 and a novel substitution (Thr-->Gly) at codon 69.Journal of virology · 2000Article
- Human immunodeficiency virus type 1 reverse transcriptase and protease mutation search engine for queries.Nature medicine · 2000Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
A variant of human immunodeficiency virus type 1 (HIV-1) possessing a deletion in the reverse transcriptase (RT) gene at codon 67 was identified in a patient who had failed combination antiretroviral therapy. This deletion initially emerged under the selective pressure of combination therapy with 3'-azido-3'-deoxythymidine (AZT) plus 2',3'-dideoxyinosine. It has persisted for more than 3 years in association with the accumulation of a variety of other well-described drug resistance mutations and an uncharacterized mutation at RT codon 69 (T69G). Phenotypic studies demonstrated that the codon 67 deletion by itself had little effect on AZT sensitivity. However, in the context of the T69G mutation and three other mutations known to be associated with AZT resistance (K70R, T215F, and K219Q), this deletion led to a increase in AZT resistance from 8. 5-fold to 445-fold. A further increase in resistance (up to 1, 813-fold) was observed when two mutations associated with nonnucleoside RT inhibitor resistance (K103N and L74I) were added to the deletion T69G K70R T215F K219Q construct. Hence, these results establish that a deletion at RT codon 67 may be selected for in the presence of antiretroviral therapy and may lead to high-level resistance to AZT.
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