Evidence map›Paper›PMID 26098993›Full record

ArticleJournal of viral hepatitis2015

Response to treatment following recently acquired hepatitis C virus infection in a multicentre collaborative cohort.

J S Doyle, K Deterding, J Grebely, H Wedemeyer, R Sacks-Davis, T Spelman, G Matthews, T M Rice, M D Morris, B H McGovern and 8 more

Abstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of viral hepatitis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. KASL clinical practice guidelines: management of hepatitis C.Clinical and molecular hepatology · 2016
    Guideline
  2. Article
  3. Review
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

18 authors.

J S DoyleCentre for Population Health, Burnet Institute, Melbourne, Vic., Australia.
K DeterdingHannover Medical School, Hannover, Germany.
J GrebelyKirby Institute, UNSW Australia, Sydney, NSW, Australia.
H WedemeyerHannover Medical School, Hannover, Germany.
R Sacks-DavisCentre for Population Health, Burnet Institute, Melbourne, Vic., Australia.
T SpelmanCentre for Population Health, Burnet Institute, Melbourne, Vic., Australia.
G MatthewsKirby Institute, UNSW Australia, Sydney, NSW, Australia.
T M RiceDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
M D MorrisDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
B H McGovernTufts Medical School, Boston, MA, USA.
A Y KimHarvard Medical School, Boston, MA, USA.
J BruneauCRCHUM, Université de Montréal, Montreal, QC, Canada.
A R LloydSchool of Medical Sciences, UNSW Australia, Sydney, NSW, Australia.
K PageDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
M P MannsHannover Medical School, Hannover, Germany.
M E HellardCentre for Population Health, Burnet Institute, Melbourne, Vic., Australia.
G J DoreKirby Institute, UNSW Australia, Sydney, NSW, Australia.
InC3 Study Group

Funding

UNM HSC Clinical and Translational Science CenterUL1TR001449 · NCATS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CAMPEN, MATTHEW J, PANDHI, NANCY · 2015 to 2024
$36.9M
Acute Hepatitis C Infection in Young InjectorsR01DA016017 · NIDA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PAGE, KIMBERLY · 2002 to 2018
$14.0M
The role of NK cells during acute HCV infection and antiviral therapyU19AI066345 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI LAUER, GEORG MICHAEL · 2005 to 2014
$8.5M
Treatment of recently acquired hepatitis C virus infectionR01DA015999 · NIDA · UNIVERSITY OF NEW SOUTH WALES · PI DORE, GREGORY JOHN · 2003 to 2014
$3.7M
Discovery and Assessment of Genetic Determinants of HCV and HIV ControlR01DA033541 · NIDA · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, RAYMOND T, KIM, ARTHUR Y · 2011 to 2015
$3.4M
International Collaborative of prospective studies of HIV and Hepatitis in IDUR01DA031056 · NIDA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PAGE, KIMBERLY · 2011 to 2015
$2.2M
Understanding the interpersonal context of HIV/HCV risk within injecting dyadsK01DA037802 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MORRIS, MEGHAN D · 2014 to 2018
$913k
Canadian Institutes of Health Research MOP-103138Canadian Institutes of Health Research MOP-210232NCATS NIH HHS UL1 TR001449NIAID NIH HHS U19 AI066345NIDA NIH HHS K01 DA037802NIDA NIH HHS R01 DA015999NIDA NIH HHS R01 DA016017NIDA NIH HHS R01 DA031056NIDA NIH HHS R01DA031056NIDA NIH HHS R01 DA033541NIDA NIH HHS R01 DA15999-01
6 · The paper itself

Abstract

Pegylated interferon therapy is highly effective in recently acquired HCV. The optimal timing of treatment, regimen and influence of host factors remains unclear. We aimed to measure sustained virological response (SVR) during recent HCV infection and identify predictors of response. Data were from five prospective cohorts of high-risk individuals in Australia, Canada, Germany and the United States. Individuals with acute or early chronic HCV who commenced pegylated interferon therapy were included. The main outcome was SVR, and predictors were assessed using logistic regression. Among 516 with documented recent HCV infection, 237 were treated (pegylated interferon n = 161; pegylated interferon/ribavirin n = 76) (30% female, median age 35 years, 56% ever injected drugs, median duration of infection 6.2 months). Sixteen per cent (n = 38) were HIV/HCV co-infected. SVR among those with HCV mono-infection was 64% by intention to treat; SVR was 68% among HCV/HIV co-infection. Independent predictors of SVR in HCV mono-infection were duration of HCV infection (the odds of SVR declined by 8% per month of infection, aOR 0.92, 95% CI 0.85-0.99, P = 0.033), IFNL4 genotype (adjusted OR 2.27, 95% CI 1.13-4.56, P = 0.021), baseline HCV RNA <400 000 IU/mL (aOR 2.06, 95% CI 1.03-4.12, P = 0.041) and age ≥40 years (vs <30: aOR 2.92, 95% CI 1.31-6.49, P = 0.009), with no difference by drug regimen, HCV genotype, symptomatic infection or gender. The effect of infection duration on odds of SVR was greater among genotype-1 infection. Interferon-based HCV treatment is highly effective in recent HCV infection. Duration of infection, IFNL4 genotype and baseline HCV RNA levels can predict virological response and may inform clinical decision-making.

Indexed as

AdultAntiviral AgentsAustraliaCanadaCoinfectionDrug Therapy, CombinationFemaleGermanyHepacivirusHepatitis C, ChronicHIV InfectionsHumansInterferon-alphaInterferon alpha-2Interferon LambdaInterleukinsAntiviral AgentsIFNL4 protein, humanInterferon-alphaInterferon alpha-2Interferon LambdaInterleukinspeginterferon alfa-2apeginterferon alfa-2bPolyethylene GlycolsRecombinant ProteinsRibavirinacute infectionhepatitis C virusrecently acquired infectionvirological response

Identifiers

PMID26098993
PMCPMC4618180

What OpenQuestion holds

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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.