ArticleAIDS reviews2000
The Genetic Basis of HIV-1 Resistance to Reverse Transcriptase and Protease Inhibitors.
Article in AIDS reviews, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Major Drug Resistance Mutations on Reverse Transcriptase Gene in Human Immunodeficiency Virus Type-1 in Indonesia: A Systematic Review.Current HIV/AIDS reports · 2024Pooled it
- The Burden of Pretreatment HIV Drug Resistance in Trinidad and Tobago.AIDS research and human retroviruses · 2024Article
- Molecular docking analysis of flavonoid compounds with HIV-1 Reverse transcriptase for the identification of potential effective inhibitors.Bioinformation · 2019Article
- Use of Proviral DNA to Investigate Virus Resistance Mutations in HIV-infected Zimbabweans.The open microbiology journal · 2017Article
- Data-intensive analysis of HIV mutations.BMC bioinformatics · 2015Article
- Genetic Consequences of Antiviral Therapy on HIV-1.Computational and mathematical methods in medicine · 2015Review
- Natural polymorphisms and unusual mutations in HIV-1 protease with potential antiretroviral resistance: a bioinformatic analysis.BMC bioinformatics · 2014Article
- What do molecules do when we are not looking? State sequence analysis for stochastic chemical systems.Journal of the Royal Society, Interface · 2012Article
- Viremia and HIV-1 drug resistance mutations among patients receiving second-line highly active antiretroviral therapy in Chennai, Southern India.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2012Article
- Investigation of Super Learner Methodology on HIV-1 Small Sample: Application on Jaguar Trial Data.AIDS research and treatment · 2012Article
- Selective pressures of HLA genotypes and antiviral therapy on human immunodeficiency virus type 1 sequence mutation at a population level.Clinical and vaccine immunology : CVI · 2007Article
- Geno2pheno: Estimating phenotypic drug resistance from HIV-1 genotypes.Nucleic acids research · 2003Article
- Rapid assessment of phenotypic resistance to protease inhibitors in human immunodeficiency virus type 1 group O.Journal of clinical microbiology · 2002Article
- Genotypic testing for human immunodeficiency virus type 1 drug resistance.Clinical microbiology reviews · 2002Review
- A Guide to HIV-1 Reverse Transcriptase and Protease Sequencing for Drug Resistance Studies.HIV sequence compendium · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 drug resistance is caused by mutations in the reverse transcriptase (RT) and protease enzymes, the molecular targets of antiretroviral therapy. At the beginning of the year 2000, two expert panels recommended that HIV-1 RT and protease susceptibility testing be used to help select antiretroviral drugs for HIV-1-infected patients. Genotypic assays have been developed to detect HIV-1 mutations known to confer antiretroviral drug resistance. Genotypic assays using dideoxynucleoside sequencing provide extensive insight into the presence of drug-resistant variants in the population of viruses within an individual. However, the interpretation of these assays in clinical settings is formidable because of the large numbers of drug resistance mutations and because these mutations interact with one another and emerge in complex patterns. In addition, cross-resistance between antiretroviral drugs is greater than that anticipated from initial in vitro studies. This review summarises the published data linking HIV-1 RT and protease mutations to in vitro and clinical resistance to the currently available nucleoside RT inhibitors, non-nucleoside RT inhibitors, and protease inhibitors.
Identifiers
19096725PMC2604813W192016177What OpenQuestion holds
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.