The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Identification of Three Interferon-Inducible Cellular Enzymes That Inhibit the Replication of Hepatitis C Virus
Open accessAbstract
Hepatitis C virus (HCV) infection is a common cause of chronic hepatitis and is currently treated with alpha interferon (IFN-α)-based therapies. However, the underlying mechanism of IFN-α therapy remains to be elucidated. To identify the cellular proteins that mediate the antiviral effects of IFN-α, we created a HEK293-based cell culture system to inducibly express individual interferon-stimulated genes (ISGs) and determined their antiviral effects against HCV. By screening 29 ISGs that are induced in Huh7 cells by IFN-α and/or up-regulated in HCV-infected livers, we discovered that viperin, ISG20, and double-stranded RNA-dependent protein kinase (PKR) noncytolytically inhibited the replication of HCV replicons. Mechanistically, inhibition of HCV replication by ISG20 and PKR depends on their 3′-5′ exonuclease and protein kinase activities, respectively. Moreover, our work, for the first time, provides strong evidence suggesting that viperin is a putative radical S-adenosyl-l-methionine (SAM) enzyme. In addition to demonstrating that the antiviral activity of viperin depends on its radical SAM domain, which contains conserved motifs to coordinate [4Fe-4S] cluster and cofactor SAM and is essential for its enzymatic activity, mutagenesis studies also revealed that viperin requires an aromatic amino acid residue at its C terminus for proper antiviral function. Furthermore, although the N-terminal 70 amino acid residues of viperin are not absolutely required, deletion of this region significantly compromises its antiviral activity against HCV. Our findings suggest that viperin represents a novel antiviral pathway that works together with other antiviral proteins, such as ISG20 and PKR, to mediate the IFN response against HCV infection.
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Cites
HOW CELLS RESPOND TO INTERFERONS
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Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus
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Hepatitis C Viral Dynamics in Vivo and the Antiviral Efficacy of Interferon-α Therapy
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Genomic analysis of the host response to hepatitis C virus infection
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Unravelling hepatitis C virus replication from genome to function
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Cited by
Interferon-stimulated genes: A complex web of host defenses
Schneider, W. M., Chevillotte, M. D., & Rice, C. M. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120231 · Cited by 3,067
Interferon-stimulated genes and their antiviral effector functions
Schoggins, J. W., & Rice, C. M. (2011) · Current Opinion in Virology · doi:10.1016/j.coviro.2011.10.008 · Cited by 1,289
Winkler, E. S., Bailey, A. L., Kafai, N. M., Nair, S., McCune, B. T., Yu, J., Fox, J. M., Chen, R. E., Earnest, J. T., Keeler, S. P., et al. (2020) · Nature Immunology · doi:10.1038/s41590-020-0778-2 · Cited by 901
Radical S-Adenosylmethionine Enzymes
Broderick, J. B., Duffus, B. R., Duschene, K. S., & Shepard, E. M. (2014) · Chemical Reviews · doi:10.1021/cr4004709 · Cited by 830
The IFITM Proteins Inhibit HIV-1 Infection
Lu, J., Pan, Q., Rong, L., Liu, S.-L., & Liang, C. (2011) · Journal of Virology · doi:10.1128/jvi.01531-10 · Cited by 417
Metadata
- Authors
- Jiang, D., Guo, H., Xu, C., Chang, J., Gu, B., Wang, L., Block, T. M., & Guo, J.-T.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2008-02-15
- Volume
- 82
- Issue
- 4
- Pages
- 1665-1678
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- OpenAlex
- W2143671051
- Cited by
- 288
- References
- 67
- FWCI
- 6.25
- Type
- journal article
- Language
- en
- Open access
- green
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