Trial reportAntimicrobial agents and chemotherapy2010
Gag mutations can impact virological response to dual-boosted protease inhibitor combinations in antiretroviral-naïve HIV-infected patients.
Trial report in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Antiretroviral Drug-Resistance Mutations on thePathogens (Basel, Switzerland) · 2022Article
- Gag P2/NC and pol genetic diversity, polymorphism, and drug resistance mutations in HIV-1 CRF02_AG- and non-CRF02_AG-infected patients in Yaoundé, Cameroon.Scientific reports · 2017Article
- High rate of HIV-1 drug resistance in treatment failure patients in Taiwan, 2009-2014.Infection and drug resistance · 2017Article
- Emerging antiretroviral drug resistance in sub-Saharan Africa: novel affordable technologies are needed to provide resistance testing for individual and public health benefits.AIDS (London, England) · 2014Article
- HIV-1 Gag C-terminal amino acid substitutions emerging under selective pressure of protease inhibitors in patient populations infected with different HIV-1 subtypes.Retrovirology · 2014Article
- Emergence of HIV drug resistance during first- and second-line antiretroviral therapy in resource-limited settings.The Journal of infectious diseases · 2013Review
- HIV-1 frameshift efficiency is primarily determined by the stability of base pairs positioned at the mRNA entrance channel of the ribosome.Nucleic acids research · 2013Article
- Mutations in multiple domains of Gag drive the emergence of in vitro resistance to the phosphonate-containing HIV-1 protease inhibitor GS-8374.Journal of virology · 2013Article
- Article
- Human Immunodeficiency Virus Gag and protease: partners in resistance.Retrovirology · 2012Review
- Effect of natural polymorphisms in the HIV-1 CRF02_AG protease on protease inhibitor hypersusceptibility.Antimicrobial agents and chemotherapy · 2012Article
- Mutational patterns in the frameshift-regulating site of HIV-1 selected by protease inhibitors.Medical microbiology and immunology · 2012Article
- Novel method for simultaneous quantification of phenotypic resistance to maturation, protease, reverse transcriptase, and integrase HIV inhibitors based on 3'Gag(p2/p7/p1/p6)/PR/RT/INT-recombinant viruses: a useful tool in the multitarget era of antiretroviral therapy.Antimicrobial agents and chemotherapy · 2011Article
- Positive impact of HIV-1 gag cleavage site mutations on the virological response to darunavir boosted with ritonavir.Antimicrobial agents and chemotherapy · 2011Article
- Three residues in HIV-1 matrix contribute to protease inhibitor susceptibility and replication capacity.Antimicrobial agents and chemotherapy · 2011Article
- Article
- Molecular Basis for Drug Resistance in HIV-1 Protease.Viruses · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ANRS 127 was a randomized pilot trial involving naïve patients receiving two dual-boosted protease inhibitor (PI) combinations. Virological response, defined as a plasma HIV RNA level of <50 copies/ml at week 16, occurred in only 41% patients. Low baseline plasma HIV RNA level was the only significant predictor of virological response. The purpose of this study was to investigate the impact on virological response of pretherapy mutations in cleavage sites of gag, gag-pol, and the gag-pol frameshift region. The whole gag gene and protease-coding region were amplified and sequenced at baseline and at week 16 for 48 patients still on the allocated regimen at week 16. No major PI resistance-associated mutations were detected either at baseline or in the 26 patients who did not achieve virological response at week 16. Baseline cleavage site substitutions in the product of the gag open reading frame at positions 128 (p17/p24) (P = 0.04) and 449 (p1/p6(gag)) (P = 0.01) were significantly more frequent in those patients not achieving virological response. Conversely, baseline cleavage site mutation at position 437 (TFP/p6(pol)) was associated with virological response (P = 0.04). In multivariate analysis adjusted for baseline viral load, these 3 substitutions remained independently associated with virological response. We demonstrated here, in vivo, an impact of baseline polymorphic gag mutations on virological response in naïve patients receiving a combination of two protease inhibitors. However, it was not possible to link the substitutions selected under PI selective pressure with virological failure.
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