ReviewAntiviral therapy2012
Epistatic connectivity among HCV genomic sites as a genetic marker of interferon resistance.
Review in Antiviral therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Quantitative differences between intra-host HCV populations from persons with recently established and persistent infections.Virus evolution · 2021Article
- Article
- Article
- Genetic host specificity of hepatitis E virus.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2014Article
- Application of mass spectrometry to molecular diagnostics of viral infections.Expert review of molecular diagnostics · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Until recently, the standard-of-care therapy of patients with HCV infection involves treatment with interferon (IFN) and ribavirin (RBV). Host demographic and genetic factors as well as HCV genetic heterogeneity have been shown to be associated with outcomes of therapy. Although resistance to IFN/RBV remains an important clinical and public health problem, there are no reliable genetic markers for the prediction of the therapy outcomes. Recently, it was shown that adaptation to IFN, a major constituent of the host innate immunity, is reflected in the HCV genetic composition and epistatic connectivity among polymorphic genomic sites, thus providing novel genetic markers of IFN resistance. Consideration of coordinated evolution among HCV genomic sites allows for identification of these genetic markers from short regions of the HCV genome and for accurate prediction of therapeutic outcomes. HCV genomic co-evolution offers a general framework for the detection of predisposition to IFN resistance, and possibly to resistance to direct-acting antivirals.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.