Evidence map›Paper›PMID 24697920›Full record

ArticleHaemophilia : the official journal of the World Federation of Hemophilia2014

Hepatitis C virus NS3 mutations in haemophiliacs.

M V Lin, A N Charlton, S D Rouster, P J Zamor, K E Sherman

Open access · greenAbstract read
In one paragraph

Article in Haemophilia : the official journal of the World Federation of Hemophilia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Viral dynamic modelling of Hepatitis C and resistance-associated variants in haemophiliacs.Haemophilia : the official journal of the World Federation of Hemophilia · 2016
    Trial
  2. Trial
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

5 authors at 2 institutions in 1 country.

M V LinUniversity of Cincinnati College of Medicine, Cincinnati, OH, USA.
A N Charlton
S D Rouster
P J Zamor
K E Sherman
University of Cincinnati Medical Center · USCarolinas Medical Center · US

Funding

PEDIATRIC GASTROENTEROLOGY AND NUTRITION TRAINING GRANTT32DK007727 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Phillip P Minar · 1995 to 2026
$11.3M
Mentorship in Liver DiseaseK24DK070528 · NIDDK · UNIVERSITY OF CINCINNATI · PI SHERMAN, KENNETH E · 2005 to 2014
$1.4M
Viral kinetic models of HCV clearance in hemophiliacs treated with telaprevirR34HL109334 · NHLBI · UNIVERSITY OF CINCINNATI · PI SHERMAN, KENNETH E · 2012 to 2013
$713k
NHLBI NIH HHS R34 HL109334NIDDK NIH HHS 5T32DK07727-15NIDDK NIH HHS K24 DK070528NIDDK NIH HHS T32 DK007727PHS HHS K24 070528
6 · The paper itself

Abstract

Haemophiliacs have high hepatitis C virus (HCV) exposure risk from blood products that did not undergo heat inactivation or disease-specific screening prior to 1987. Repeated exposure to infected factor concentrates predisposes haemophiliacs to higher likelihood of HCV from multiple sources. HIV coinfection could result in impaired clearance of less fit variants resulting in enrichment of quasispecies carrying resistance mutations. We postulated that haemophiliacs demonstrate increased prevalence of baseline signature mutations in the HCV NS3/4 serine protease coding domain. We examined the prevalence of putative HCV protease inhibitor mutations, mutations, subclassified into dominant mutations if changes conferred resistance, and minor variants not associated with drug resistance, in patients with haemophilia A or B, infected with HCV or HCV/HIV, prior to HCV PI exposure. A total of 151 subjects were evaluated, including 22 haemophiliacs and 129 non-haemophilic controls. Of the 58 mutations detected, 55 (95%) were resistance mutations and three (5%) were minor variants. Dominant mutations were detected in 10 (45.5%) haemophiliacs and in 43 (33.3%) controls (OR 1.67, 95% CI 0.67-4.16). There was no statistical difference in proportion of dominant mutations (P = 0.27) or minor variants (P = 0.47) between groups, despite adjustment for HIV status (P = 0.44). No significant differences in dominant or minor resistance mutations between haemophiliacs and non-haemophiliacs were observed. HIV presence or prior HAART exposure did not affect baseline distribution. We conclude that haemophiliacs are not at higher risk for pre-existing HCV PI mutations, and prospective studies of response to PI-based regimens with HCV activity are indicated.

Indexed as

AdolescentAdultAnalysis of VarianceAntiviral AgentsCase-Control StudiesCoinfectionDEAD-box RNA HelicasesDrug Resistance, ViralFemaleGenotypeHemophilia AHemophilia BHepacivirusHepatitis CHIV InfectionsHumansAntiviral AgentsDEAD-box RNA HelicasesNS3 protein, hepatitis C virusNucleoside-TriphosphataseProtease InhibitorsRNA, ViralSerine EndopeptidasesViral Nonstructural ProteinsViral ProteasesHCVinherited bleeding disordersmutationNS3protease

Identifiers

PMID24697920
PMCPMC4149859
OpenAlexW2122004242

What OpenQuestion holds

Textmetadata
LicenceTDM
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.