Evidence map›Paper›PMID 27685471›Full record

ArticlePloS one

NS3 Resistance-Associated Variants (RAVs) in Patients Infected with HCV Genotype 1a in Spain.

María Ángeles Jimenez-Sousa, Mónica Gutiérrez-Rivas, Alejandro Álvaro-Meca, Mónica García-Álvarez, P Richard Harrigan, Cesare Giovanni Fedele, Verónica Briz, Sonia Vázquez-Morón, Salvador Resino

Open access · goldAbstract read
In one paragraph

Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

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  7. Antimicrobial agents and chemotherapy · 2018
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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

9 authors at 3 institutions in 2 countries.

María Ángeles Jimenez-SousaViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Mónica Gutiérrez-RivasViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Alejandro Álvaro-MecaPreventive Medicine and Public Health Unit, Faculty of Health Sciences, Rey Juan Carlos College, Alcorcón, Madrid, Spain.
Mónica García-ÁlvarezViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
P Richard HarriganBritish Columbia Centre for Excellence in HIV/AIDS, Vancouver, Canada.
Cesare Giovanni FedeleDiagnostic Approach Area, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Verónica BrizViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Sonia Vázquez-MorónViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.ORCID http://orcid.org/0000-0002-0977-741X
Salvador ResinoViral Infection and Immunity Unit, National Centre for Microbiology. Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Instituto de Salud Carlos III · ESAIDS Vancouver · CAUniversidad Rey Juan Carlos · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundResistance-associated variants have been related to treatment failure of hepatitis C virus (HCV) therapy with direct-acting antiviral drugs. The aim of our study was to analyze the prevalence of clinically relevant resistance-associated variants within NS3 in patients infected with HCV genotype 1a (GT1a) in Spain.

methodsWe performed a cross-sectional study on 2568 patients from 115 hospitals throughout Spain (2014-2015). The viral NS3 protease gene was amplified by nested polymerase chain reaction and sequenced by Sanger sequencing using an ABI PRISM 377 DNA sequencer. Additionally, clade information for genotype 1a was obtained by using the software geno2pheno (http://hcv.geno2pheno.org/).

resultsIn total, 875 out of 2568 samples were from human immunodeficiency virus (HIV)/HCV-coinfected patients. Q80K was the main RAV found in our patients (11.1%) and the rest of the resistance-associated variants had a lower frequency, including S122G (6.23%), T54S (3.47%), V55A (2.61%), and V55I (2.15%), which were among the most frequent after Q80K. Overall, 286 samples had the Q80K polymorphism (11.1%) and 614 (23.9%) were GT1a clade I. HIV/HCV-coinfected patients had a higher frequency of Q80K and GT1a clade I than HCV-monoinfected patients (12.9% vs. 9.6% [p = 0.012] and 28.5% vs. 21.4% [p<0.001], respectively). Both the prevalence of Q80K and GT1a clade I were not uniform throughout the country (p<0.001), which ranged from 7.3%-22.2% and 15.7%-42.5%, respectively. The frequency of the Q80K polymorphism was far higher in patients infected with GT1a clade I than in patients infected with GT1a clade II (41.5% vs. 1.6%; p<0.001).

conclusionsThe prevalence of most resistance-associated variants in NS3 was low in patients infected with HCV GT1a in Spain, except for Q80K (11.1%), which was also notably higher in HIV/HCV-coinfected patients. The vast majority of Q80K polymorphisms were detected in GT1a clade I.

Identifiers

PMID27685471
PMCPMC5042525
OpenAlexW2525816050

What OpenQuestion holds

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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.