Evidence map›Paper›PMID 11060045›Full record

ArticleJournal of clinical microbiology2000

Genetic diversity of protease and reverse transcriptase sequences in non-subtype-B human immunodeficiency virus type 1 strains: evidence of many minor drug resistance mutations in treatment-naive patients.

L Vergne, M Peeters, E Mpoudi-Ngole, A Bourgeois, F Liegeois, C Toure-Kane, S Mboup, C Mulanga-Kabeya, E Saman, J Jourdan and 2 more

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In one paragraph

Article in Journal of clinical microbiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 186 citations in OpenAlex.

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  8. On the contribution of Angola to the initial spread of HIV-1.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2016
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  19. Critical differences in HIV-1 and HIV-2 protease specificity for clinical inhibitors.Protein science : a publication of the Protein Society · 2012
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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

12 authors at 5 institutions in 3 countries.

L VergneLaboratoire Retrovirus, IRD, Montpellier, France.
M Peeters
E Mpoudi-Ngole
A Bourgeois
F Liegeois
C Toure-Kane
S Mboup
C Mulanga-Kabeya
E Saman
J Jourdan
J Reynes
E Delaporte
Institut de Recherche pour le Développement · FRHôpital Aristide Le Dantec · SNHôpital Gui de Chauliac · FRCentre Hospitalier Universitaire de Nîmes · FRFujirebio (Belgium) · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most human immunodeficiency virus (HIV) drug susceptibility studies have involved subtype B strains. Little information on the impact of viral diversity on natural susceptibility to antiretroviral drugs has been reported. However, the prevalence of non-subtype-B (non-B) HIV type 1 (HIV-1) strains continues to increase in industrialized countries, and antiretroviral treatments have recently become available in certain developing countries where non-B subtypes predominate. We sequenced the protease and reverse transcriptase (RT) genes of 142 HIV-1 isolates from antiretroviral-naive patients: 4 belonged to group O and 138 belonged to group M (9 subtype A, 13 subtype B, 2 subtype C, 5 subtype D, 2 subtype F1, 9 subtype F2, 4 subtype G, 5 subtype J, 2 subtype K, 3 subtype CRF01-AE, 67 subtype CRF02-AG, and 17 unclassified isolates). No major mutations associated with resistance to nucleoside reverse transcriptase inhibitors (NRTIs) or protease inhibitors were detected. Major mutations linked to resistance to non-NRTI agents were detected in all group O isolates (A98G and Y181C) and in one subtype J virus (V108I). In contrast, many accessory mutations were found, especially in the protease gene. Only 5.6% of the 142 strains, all belonging to subtype B or D, had no mutations in the protease gene. Sixty percent had one mutation, 22.5% had two mutations, 9.8% had three mutations, and 2.1% (all group O strains) had four mutations. In order of decreasing frequency, the following mutations were identified in the protease gene: M36I (86.6%), L10I/V (26%), L63P (12.6%), K20M/R (11.2%), V77I (5.6%), A71V (2.8%), L33F (0.7%), and M46I (0.7%). R211K, an accessory mutation associated with NRTI resistance, was also observed in 43.6% of the samples. Phenotypic and clinical studies are now required to determine whether multidrug-resistant viruses emerge more rapidly during antiretroviral therapy when minor resistance-conferring mutations are present before treatment initiation.

Indexed as

Genetic VariationAmino Acid SequenceDrug Resistance, MicrobialHIV-1HIV InfectionsHIV ProteaseHIV Reverse TranscriptaseHumansMolecular Sequence DataMutationPhylogenyPolymerase Chain ReactionSequence AlignmentHIV ProteaseHIV Reverse Transcriptase

Identifiers

PMID11060045
PMCPMC87518
OpenAlexW2106448315

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Registered trials

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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.