ArticleAIDS (London, England)2009
Genetic determinants in HIV-1 Gag and Env V3 are related to viral response to combination antiretroviral therapy with a protease inhibitor.
Article in AIDS (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Phenotypic characterization of virological failure following lopinavir/ritonavir monotherapy using full-length Gag-protease genes.The Journal of antimicrobial chemotherapy · 2014Article
- Empirical validation of viral quasispecies assembly algorithms: state-of-the-art and challenges.Scientific reports · 2013Article
- High-resolution deep sequencing reveals biodiversity, population structure, and persistence of HIV-1 quasispecies within host ecosystems.Retrovirology · 2012Article
- The HIV-1 protease inhibitor nelfinavir activates PP2 and inhibits MAPK signaling in macrophages: a pathway to reduce inflammation.Journal of leukocyte biology · 2012Article
- A cleavage enzyme-cytometric bead array provides biochemical profiling of resistance mutations in HIV-1 Gag and protease.Biochemistry · 2011Article
- Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy.AIDS (London, England) · 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
11 authors.
Funding
Abstract
objectiveTo identify novel viral determinants in HIV-1 protease, Gag, and envelope V3 that relate to outcomes to initial protease inhibitor-based antiretroviral therapy.
designA longitudinal cohort study of protease inhibitor-naive, HIV-infected individuals was designed to identify genetic variables in viral Gag and envelope sequences associated with response to antiretroviral therapy.
methodsGenetic and statistical models, including amino acid profiles, phylogenetic analyses, receiver operating characteristic analyses, and covariation analyses, were used to evaluate viral sequences and clinical variables from individuals who developed immune reconstitution with or without suppression of viral replication.
resultsPretherapy chemokine (C-X-C motif) receptor 4-using V3 regions had significant associations with viral failure (P = 0.04). Amino acid residues in protease covaried with Gag residues, particularly in p7(NC), independent of cleavage sites. Pretherapy V3 charge combined with p6(Pol) and p2/p7(NC) cleavage site genotypes produced the best three-variable model to predict viral suppression in 88% of individuals. Combinations of baseline CD4 cell percentage with genetic determinants in Gag-protease predicted viral fitness in 100% of individuals who failed to suppress viral replication.
conclusionBaseline genetic determinants in Gag p6(Pol) and p2/p7(NC), as well as envelope, provide novel combinations of biomarkers for predicting emergence of viral resistance to initial therapy regimens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.