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Understanding the hepatitis C virus life cycle paves the way for highly effective therapies
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More than two decades of intense research has provided a detailed understanding of hepatitis C virus (HCV), which chronically infects 2% of the world's population. This effort has paved the way for the development of antiviral compounds to spare patients from life-threatening liver disease. An exciting new era in HCV therapy dawned with the recent approval of two viral protease inhibitors, used in combination with pegylated interferon-α and ribavirin; however, this is just the beginning. Multiple classes of antivirals with distinct targets promise highly efficient combinations, and interferon-free regimens with short treatment duration and fewer side effects are the future of HCV therapy. Ongoing and future trials will determine the best antiviral combinations and whether the current seemingly rich pipeline is sufficient for successful treatment of all patients in the face of major challenges, such as HCV diversity, viral resistance, the influence of host genetics, advanced liver disease and other co-morbidities.
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Structural Determinants That Target the Hepatitis C Virus Core Protein to Lipid Droplets
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Structure of the catalytic domain of the hepatitis C virus NS2-3 protease
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Molecular Determinants and Dynamics of Hepatitis C Virus Secretion
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Cell Culture Adaptation of Hepatitis C Virus and In Vivo Viability of an Adapted Variant
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Hepatitis C virus induces interferon-λ and interferon-stimulated genes in primary liver cultures
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Self-citationStructure of a Pestivirus Envelope Glycoprotein E2 Clarifies Its Role in Cell Entry
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Self-citationCurrent progress in development of hepatitis C virus vaccines
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Self-citationTrafficking of Hepatitis C Virus Core Protein during Virus Particle Assembly
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Self-citationGenotype-dependent sensitivity of hepatitis C virus to inhibitors of the p7 ion channel
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Hepatitis C Virus Is Primed by CD81 Protein for Low pH-dependent Fusion
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Self-citationHCV and the hepatic lipid pathway as a potential treatment target
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Metadata
- Authors
- Scheel, T. K. H., & Rice, C. M.
- Venue
- Nature Medicine
- Published
- 2013-07
- Volume
- 19
- Issue
- 7
- Pages
- 837-849
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2024763248
- Cited by
- 554
- References
- 133
- FWCI
- 49.00
- Type
- journal article
- Language
- en
- Open access
- green
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
