Evidence map›Paper›PMID 15731227›Full record

Trial reportJournal of virology2005

Selection of resistance in protease inhibitor-experienced, human immunodeficiency virus type 1-infected subjects failing lopinavir- and ritonavir-based therapy: mutation patterns and baseline correlates.

Hongmei Mo, Martin S King, Kathryn King, Akhteruzzaman Molla, Scott Brun, Dale J Kempf

Open access · greenAbstract readClinical TrialClinical Trial, Phase IIClinical Trial, Phase III
In one paragraph

Trial report in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. 2022 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. 2019 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 2011 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2011
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hongmei MoDepartment R47D, Building AP52N, Abbott Laboratories, 200 Abbott Park Rd., Abbott Park, IL 60064-6217, USA. Hongmei.Mo@abbott.com
Martin S King
Kathryn King
Akhteruzzaman Molla
Scott Brun
Dale J Kempf
Abbott Fund · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The selection of in vivo resistance to lopinavir was characterized by analyzing the longitudinal isolates from 54 protease inhibitor-experienced subjects who either experienced incomplete virologic response or viral rebound subsequent to initial response while on treatment with lopinavir-ritonavir in Phase II and III studies. The evolution of incremental resistance to lopinavir (emergence of new mutation[s] and/or at least a twofold increase in phenotypic resistance compared to baseline isolates) was highly dependent on the baseline phenotype and genotype. Among the subjects demonstrating evolution of lopinavir resistance, mutations at positions 82, 54, and 46 in human immunodeficiency virus protease emerged frequently, suggesting that these mutations are important for conferring high-level resistance. Less common mutations, such as L33F, I50V, and V32I together with I47V/A, were also selected; however, new mutations at positions 84, 90, and 71 were not observed. The emergence of incremental resistance contrasts greatly with the low incidence of resistance observed after initiating lopinavir-ritonavir therapy in antiretroviral-naive patients, suggesting that partial resistance accumulated during prior protease inhibitor therapy can compromise the genetic barrier to resistance to lopinavir-ritonavir. The emergence of incremental resistance was uncommon in subjects whose baseline isolates contained eight or more mutations associated with lopinavir resistance and/or displayed >60-fold-reduced susceptibility to lopinavir, providing insight into suitable upper genotypic and phenotypic breakpoints for lopinavir-ritonavir.

Indexed as

Amino Acid SubstitutionDrug Resistance, ViralDrug Therapy, CombinationGenotypeHIV-1HIV InfectionsHIV ProteaseHIV Protease InhibitorsHumansLopinavirMicrobial Sensitivity TestsMutationPyrimidinonesReverse Transcriptase InhibitorsRitonavirRNA, ViralHIV ProteaseHIV Protease InhibitorsLopinavirPyrimidinonesReverse Transcriptase InhibitorsRitonavirRNA, Viral

Identifiers

PMID15731227
PMCPMC1075714
OpenAlexW2090394672

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.