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Science 2 July 1999:
Vol. 285. no. 5424, pp. 107 - 110
DOI: 10.1126/science.285.5424.107
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Reports

Inhibition of the Interferon- Inducible Protein Kinase PKR by HCV E2 Protein

Deborah R. Taylor, 1 Stephanie T. Shi, 1 Patrick R. Romano, 3 Glen N. Barber, 4 Michael M. C. Lai 12*

Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2alpha , a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.

1 Department of Molecular Microbiology and Immunology and
2 Howard Hughes Medical Institute, University of Southern California, School of Medicine, Los Angeles, CA 90089, USA.
3 Small Molecule Therapeutics, Monmouth Junction, NJ 08852, USA.
4 University of Miami, School of Medicine, Miami, FL 33136, USA.
*   To whom correspondence should be addressed. E-mail: michlai{at}hsc.usc.edu

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Activation of the Interferon-Inducible 2'-5'-Oligoadenylate Synthetase Gene by Hepatitis C Virus Core Protein.
A. Naganuma, A. Nozaki, T. Tanaka, K. Sugiyama, H. Takagi, M. Mori, K. Shimotohno, and N. Kato (2000)
J. Virol. 74, 8744-8750
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Evasion of Host Defenses by Measles Virus: Wild-Type Measles Virus Infection Interferes with Induction of Alpha/Beta Interferon Production.
D. Naniche, A. Yeh, D. Eto, M. Manchester, R. M. Friedman, and M. B. A. Oldstone (2000)
J. Virol. 74, 7478-7484
   Abstract »    Full Text »
Replication of hepatitis C virus.
R. Bartenschlager and V. Lohmann (2000)
J. Gen. Virol. 81, 1631-1648
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Expression of Hepatitis C Virus Proteins Interferes with the Antiviral Action of Interferon Independently of PKR-Mediated Control of Protein Synthesis.
C. François, G. Duverlie, D. Rebouillat, H. Khorsi, S. Castelain, H. E. Blum, A. Gatignol, C. Wychowski, D. Moradpour, and E. F. Meurs (2000)
J. Virol. 74, 5587-5596
   Abstract »    Full Text »
Liver-Specific Alpha 2 Interferon Gene Expression Results in Protection from Induced Hepatitis.
L. Aurisicchio, P. Delmastro, V. Salucci, O. G. Paz, P. Rovere, G. Ciliberto, N. La Monica, and F. Palombo (2000)
J. Virol. 74, 4816-4823
   Abstract »    Full Text »
Microarray Analysis Identifies Interferon-Inducible Genes and Stat-1 as Major Transcriptional Targets of Human Papillomavirus Type 31.
Y. E. Chang and L. A. Laimins (2000)
J. Virol. 74, 4174-4182
   Abstract »    Full Text »
Hepatitis C Virus NS5A Protein Modulates Transcription through a Novel Cellular Transcription Factor SRCAP.
A. K. Ghosh, M. Majumder, R. Steele, P. Yaciuk, J. Chrivia, R. Ray, and R. B. Ray (2000)
J. Biol. Chem. 275, 7184-7188
   Abstract »    Full Text »    PDF »
Hepatitis C Virus, the E2 Envelope Protein, and -Interferon Resistance.
K. Abid, R. Quadri, F. Negro;, D. R. Taylor, S. T. Shi, P. R. Romano, G. N. Barber, and M. M. Lai; (2000)
Science 287, 1555a-1555
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Pathogenesis, Natural History, Treatment, and Prevention of Hepatitis C.
T. J. Liang, B. Rehermann, L. B. Seeff, and J. H. Hoofnagle (2000)
Ann Intern Med 132, 296-305
   Abstract »    Full Text »    PDF »
Alpha/Beta Interferons Potentiate Virus-Induced Apoptosis through Activation of the FADD/Caspase-8 Death Signaling Pathway.
S. Balachandran, P. C. Roberts, T. Kipperman, K. N. Bhalla, R. W. Compans, D. R. Archer, and G. N. Barber (2000)
J. Virol. 74, 1513-1523
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Genetic Heterogeneity of Hypervariable Region 1 of the Hepatitis C Virus (HCV) Genome and Sensitivity of HCV to Alpha Interferon Therapy.
K. Sandres, M. Dubois, C. Pasquier, J. L. Payen, L. Alric, M. Duffaut, J. P. Vinel, J. P. Pascal, J. Puel, and J. Izopet (2000)
J. Virol. 74, 661-668
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Double-stranded RNA-activated protein kinase mediates virus-induced apoptosis: A new role for an old actor.
R. J. Kaufman (1999)
PNAS 96, 11693-11695
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Hepatitis C Virus Core Protein Enhances p53 Function through Augmentation of DNA Binding Affinity and Transcriptional Ability.
M. Otsuka, N. Kato, K.-H. Lan, H. Yoshida, J. Kato, T. Goto, Y. Shiratori, and M. Omata (2000)
J. Biol. Chem. 275, 34122-34130
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Characterization of Two Evolutionarily Conserved, Alternatively Spliced Nuclear Phosphoproteins, NFAR-1 and -2, That Function in mRNA Processing and Interact with the Double-stranded RNA-dependent Protein Kinase, PKR.
L. R. Saunders, D. J. Perkins, S. Balachandran, R. Michaels, R. Ford, A. Mayeda, and G. N. Barber (2001)
J. Biol. Chem. 276, 32300-32312
   Abstract »    Full Text »    PDF »
Regulation of PKR and IRF-1 during hepatitis C virus RNA replication.
J. Pflugheber, B. Fredericksen, R. Sumpter Jr., C. Wang, F. Ware, D. L. Sodora, and M. Gale Jr. (2002)
PNAS 99, 4650-4655
   Abstract »    Full Text »    PDF »
Hepatitis C virus replication is directly inhibited by IFN-alpha in a full-length binary expression system.
R. T. Chung, W. He, A. Saquib, A. M. Contreras, R. J. Xavier, A. Chawla, T. C. Wang, and E. V. Schmidt (2001)
PNAS 98, 9847-9852
   Abstract »    Full Text »    PDF »


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