Evidence map›Paper›PMID 19644383›Full record

ArticleJournal of acquired immune deficiency syndromes (1999)2009

Clinical and genotypic findings in HIV-infected patients with the K65R mutation failing first-line antiretroviral therapy in Nigeria.

Claudia A Hawkins, Beth Chaplin, John Idoko, Ernest Ekong, Isaac Adewole, Wadzani Gashau, Robert L Murphy, Phyllis Kanki, APIN Plus/Harvard PEPFAR Team

Abstract read
In one paragraph

Article in Journal of acquired immune deficiency syndromes (1999), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Observational
  2. Article
  3. 2022 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2022
    Article
  4. 2019 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 2011 update of the drug resistance mutations in HIV-1.Topics in antiviral medicine · 2011
    Review
  17. Update on human immunodeficiency virus (HIV)-2 infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2011
    Review
  18. Article
  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

9 authors.

Claudia A HawkinsNorthwestern University, Chicago, IL 60611, USA. c-hawkins@md.northwestern.edu
Beth Chaplin
John Idoko
Ernest Ekong
Isaac Adewole
Wadzani Gashau
Robert L Murphy
Phyllis Kanki
APIN Plus/Harvard PEPFAR Team

Funding

WOMEN'S HEALTH AGENDAU01AI025915 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MURPHY, ROBERT L. · 1987 to 2006
$15.3M
NIAID NIH HHS U01 AI025915NIAID NIH HHS UO1 AI025915PHS HHS U51HA02522
6 · The paper itself

Abstract

introductionThe HIV-1 epidemic in African countries is largely due to non-B HIV-1 subtypes. Patterns and frequency of antiretroviral drug resistance mutations observed in these countries may differ from those in the developed world, where HIV-1 subtype B predominates.

methodsHIV-1 subtype and drug resistance mutations were assayed among Nigerian patients with treatment failure on first-line therapy (plasma HIV RNA >1000 copies/mL). Sequence analysis of the reverse transcriptase and protease gene revealed drug resistance mutations and HIV-1 viral subtype. Specific patterns of mutations and clinical characteristics are described in patients with the K65R mutation.

resultsSince 2005, 338 patients were evaluated. The most prevalent subtypes were CRF02_AG [152 of 338 (44.9%)] and G [128 of 338 (37.9%)]. Three hundred seven of 338 (90.8%) patients had previously received stavudine and/or zidovudine + lamivudine + efavirenz or nevirapine; 41 of 338 (12.1%) had received tenofovir (TDF). The most common nucleoside reverse transcriptase inhibitor mutations observed were M184V (301, 89.1%) and K70R (91, 26.9%). The K65R mutation was present in 37 of 338 patients (10.9%). The Q151M (P < 0.05), K219R, and T69del (P < 0.01) mutations were more common in patients with K65R who had not received TDF.

conclusionsThe K65R mutation is increasingly recognized and is a challenging finding among patients with non-B HIV subtypes, whether or not they have been exposed to TDF.

Indexed as

Antiretroviral Therapy, Highly ActiveDrug Resistance, ViralMutation, MissenseAdultAmino Acid SubstitutionAnti-HIV AgentsGenotypeHIV-1HIV InfectionsHIV ProteaseHIV Reverse TranscriptaseHumansMolecular Sequence DataNigeriaSequence Analysis, DNATreatment FailureAnti-HIV AgentsHIV ProteaseHIV Reverse Transcriptasep16 protease, Human immunodeficiency virus 1

Identifiers

PMID19644383
PMCPMC2815152

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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.