ArticleScientific reports2016
Copy number variation of genes involved in the hepatitis C virus-human interactome.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Investigating Intraspecific Diversity of Metabolic Gene Clusters with MLPA and Synthetic Probes.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Digital PCR in Virology: Current Applications and Future Perspectives.Molecular diagnosis & therapy · 2025Review
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- Birth and death of Mx genes and the presence/absence of genes regulating Mx transcription are correlated with the diversity of anti-pathogenicity in vertebrate species.Molecular genetics and genomics : MGG · 2019Article
- Article
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5 authors.
Funding
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Abstract
Copy number variation (CNV) is a newly discovered form of intra-species genetic polymorphism that is defined as deletions or duplications of genome segments ranging from 1 kbp to several Mbp. CNV accounts for the majority of the genetic variation observed in humans (CNV regions cover more than 10% of the human genome); therefore, it may significantly influence both the phenotype and susceptibility to various diseases. Unfortunately, the impact of CNV on a number of diseases, including hepatitis C virus (HCV) infection, remains largely unexplored. Here, we analyzed 421 human genes encoding proteins that have been shown to interact with HCV proteins or genomic RNA (proteins from the HCV-human interactome). We found that 19 of the 421 candidate genes are located in putative CNV regions. For all of these genes, copy numbers were determined for European, Asiatic and African populations using the multiplex ligation-dependent amplification (MLPA) method. As a result, we identified 4 genes, IGLL1, MLLT4, PDPK1, PPP1R13L, for which the CN-genotype ranged from 1 to 6. All of these genes are involved in host-virus interaction; thus, their polymorphism has a potential impact on the development of HCV infection and/or therapy outcome.
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