Evidence map›Paper›PMID 11880402›Full record

ArticleJournal of clinical microbiology2002

Human immunodeficiency virus type 1 group m protease in cameroon: genetic diversity and protease inhibitor mutational features.

Peter N Fonjungo, Eitel N Mpoudi, Judith N Torimiro, George A Alemnji, Laura T Eno, Esther J Lyonga, John N Nkengasong, Renu B Lal, Mark Rayfield, Marcia L Kalish and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of clinical microbiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Evaluation of the performance of the Cepheid Xpert HIV-1 Viral Load Assay for quantitative and diagnostic uses.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2020
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  12. Current status of HIV/AIDS in Cameroon: how effective are control strategies?International journal of environmental research and public health · 2008
    Article
  13. Article
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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 2 institutions in 2 countries.

Peter N FonjungoHIV and Retrovirology Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases, Atlanta, Georgia 30333, USA.
Eitel N Mpoudi
Judith N Torimiro
George A Alemnji
Laura T Eno
Esther J Lyonga
John N Nkengasong
Renu B Lal
Mark Rayfield
Marcia L Kalish
Thomas M Folks
Danuta Pieniazek
National Center for HIV/AIDS Viral Hepatitis STD and TB Prevention · USNational Center for Infectious Diseases · US

Funding

TUBERCULOSIS INTERNATIONAL TRAINING AND RESEARCH PROGRAMD43TW000010 · FIC · JOHNS HOPKINS UNIVERSITY · PI BEYRER, CHRISTOPHER C. · 1988 to 2012
$19.8M
FIC NIH HHS D43 TW000010
6 · The paper itself

Abstract

To establish a baseline for monitoring resistance to protease inhibitors (PIs) and examining the efficacy of their use among persons in Cameroon infected with human immunodeficiency virus type 1 (HIV-1), we analyzed genetic variability and PI resistance-associated substitutions in PCR-amplified protease (PR) sequences in strains isolated from 110 HIV-1-infected, drug-naïve Cameroonians. Of the 110 strains, 85 were classified into six HIV-1 PR subtypes, A (n = 1), B (n = 1), F (n = 4), G (n = 7), H (n = 1), and J (n = 7), and a circulating recombinant form, CRF02-AG (n = 64). PR genes from the remaining 25 (23%) specimens were unclassifiable, whereas 2% (7 of 301) unclassifiable PR sequences were reported for a global collection. Two major PI resistance-associated mutations, 20M and 24I, were detected in strains from only two specimens, whereas secondary mutations were found in strains from all samples except one strain of subtype B and two strains of CRF02-AG. The secondary mutations showed the typical PI resistance-associated pattern for non-subtype B viruses in both classifiable and unclassifiable PR genes, with 36I being the predominant (99%) mutation, followed by 63P (18%), 20R (15%), 77I (13%), and 10I or 10V (11%). Of these mutations, dual and triple PI resistance-associated substitutions were found in 38% of all the Cameroonian strains. Compared with classifiable PR sequences, unclassifiable sequences had significantly more dual and triple substitutions (64% versus 30%; P = 0.004). Phenotypic and clinical evaluations are needed to estimate whether PI resistance during antiretroviral drug treatment occurs more rapidly in individuals infected with HIV-1 strains harboring multiple PI resistance-associated substitutions. This information may be important for determination of appropriate drug therapies for HIV-1-infected persons in Cameroon, where more than one-third of HIV-1 strains were found to carry dual and triple minor PI resistance-associated mutations.

Indexed as

MutationAmino Acid SequenceDNA, ViralDrug Resistance, ViralGenetic VariationHIV-1HIV ProteaseHIV Protease InhibitorsHumansMolecular Sequence DataPhylogenyDNA, ViralHIV ProteaseHIV Protease Inhibitors

Identifiers

PMID11880402
PMCPMC120267
OpenAlexW1995267885

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.