ArticleJournal of virology2007
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.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Phenotype, Genotype, and Drug Resistance in Subtype C HIV-1 Infection.The Journal of infectious diseases · 2016Article
- Article
- 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
- Impact of HIV type 1 subtype on drug resistance mutations in Nigerian patients failing first-line therapy.AIDS research and human retroviruses · 2011Article
- Early virologic failure and the development of antiretroviral drug resistance mutations in HIV-infected Ugandan children.Journal of acquired immune deficiency syndromes (1999) · 2011Article
- Case report of the rare deletion at codon 69 of reverse transcriptase in a South African HIV-1 subtype C infected patient.Virus genes · 2010Article
- Impaired replication capacity of acute/early viruses in persons who become HIV controllers.Journal of virology · 2010Article
- Thymidine analogue resistance suppression by V75I of HIV-1 reverse transcriptase: effects of substituting valine 75 on stavudine excision and discrimination.The Journal of biological chemistry · 2009Article
- 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
- Effect of the human immunodeficiency virus type 1 reverse transcriptase polymorphism Leu-214 on replication capacity and drug susceptibility.Journal of virology · 2009Article
- Contribution of immunological and virological factors to extremely severe primary HIV type 1 infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2009Article
- Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletions, insertions, and amino acid substitutions in the beta3-beta4 hairpin loop-coding region of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been associated with resistance to nucleoside RT inhibitors when appearing in combination with other mutations in the RT-coding region. In this work, we have measured the in vivo fitness of HIV-1 variants containing a deletion of 3 nucleotides affecting codon 69 (Delta69) of the viral RT as well as the replication capacity (RC) ex vivo of a series of recombinant HIV-1 variants carrying an RT bearing the Delta69 deletion or the T69A mutation in a multidrug-resistant (MDR) sequence background, including the Q151M complex and substitutions M184V, K103N, Y181C, and G190A. Patient-derived viral clones having RTs with Delta69 together with S163I showed increased RCs under drug pressure. These data were consistent with the viral population dynamics observed in a long-term-treated HIV-1-infected patient. In the absence of drugs, viral clones containing T69A replicated more efficiently than those having Delta69, but only when patient-derived sequences corresponding to RT residues 248 to 527 were present. These effects could be attributed to a functional interaction between the C-terminal domain of the p66 subunit (RNase H domain) and the DNA polymerase domain of the RT. Finally, recombinant HIV-1 clones bearing RTs with MDR-associated mutations, including deletions at codon 69, showed increased susceptibilities to protease inhibitors in phenotypic assays. These effects correlated with impaired Gag cleavage and could be attributed to delayed maturation and decreased production of active protease in those variants.
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