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Article ; Online: Interferon-λ in HCV Infection and Therapy.

Pagliaccetti, Nicole E / Robek, Michael D

2010 Volume 2, Issue 8, Page(s) 1589–1602

Abstract: Chronic infection with hepatitis C virus (HCV) is associated with significant liver disease and is therefore an important public health problem. The current standard-of-care therapy for chronic HCV infection consists of a combination of pegylated (PEG) ... ...

Abstract	Chronic infection with hepatitis C virus (HCV) is associated with significant liver disease and is therefore an important public health problem. The current standard-of-care therapy for chronic HCV infection consists of a combination of pegylated (PEG) interferon (IFN)-α and ribavirin. Although this therapy effectively generates a sustained viral response in approximately half of treated individuals, it is associated with significant hematological and neurological side effects. A new family of IFN-related proteins (IFN-λ1, 2, and 3; or alternately, IL-29, 28A, 28B, respectively) possesses properties that may make these cytokines superior to PEG-IFN-α for HCV therapy. Genetic studies have also implicated these proteins in both the natural and therapy-induced resolution of HCV infection. This review summarizes the basic aspects of IFN-λ biology, the potential role of these cytokines in HCV infection, and the outlook for their therapeutic application.
Language	English
Publishing date	2010-08-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v2081589
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Interferon-lambda in the immune response to hepatitis B virus and hepatitis C virus.

Pagliaccetti, Nicole E / Robek, Michael D

Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

2010 Volume 30, Issue 8, Page(s) 585–590

Abstract: Approximately 500 million people worldwide are chronically infected with the hepatitis B virus (HBV) or hepatitis C virus (HCV), and are therefore at an increased risk for developing fatal liver diseases such as cirrhosis and hepatocellular carcinoma. ... ...

Abstract	Approximately 500 million people worldwide are chronically infected with the hepatitis B virus (HBV) or hepatitis C virus (HCV), and are therefore at an increased risk for developing fatal liver diseases such as cirrhosis and hepatocellular carcinoma. The intracellular antiviral responses induced by interferon (IFN)-alpha/-beta and/or IFN-gamma play critical roles in the pathogenesis of HBV and HCV infection, and the function of IFN-lambda in the host immune response to these viruses is beginning to be revealed. A better understanding of how IFN-lambda influences HBV or HCV persistence is not only important for understanding the mechanisms of chronic virus infection, but also may lead to new approaches for improved antiviral therapies.
MeSH term(s)	Animals ; Antiviral Agents/therapeutic use ; Carcinoma, Hepatocellular/epidemiology ; Comorbidity ; Cytokines/immunology ; Cytokines/therapeutic use ; Hepacivirus/immunology ; Hepatitis B virus/immunology ; Hepatitis B, Chronic/drug therapy ; Hepatitis B, Chronic/epidemiology ; Hepatitis B, Chronic/immunology ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/epidemiology ; Hepatitis C, Chronic/immunology ; Humans ; Immunity, Innate ; Liver Cirrhosis/epidemiology ; Mice ; Prevalence
Chemical Substances	Antiviral Agents ; Cytokines ; interferon-lambda protein, mouse
Language	English
Publishing date	2010-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1226675-9
ISSN	1557-7465 ; 1079-9907
ISSN (online)	1557-7465
ISSN	1079-9907
DOI	10.1089/jir.2010.0060
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Article ; Online: Inhibition of type III interferon activity by orthopoxvirus immunomodulatory proteins.

Bandi, Prasanthi / Pagliaccetti, Nicole E / Robek, Michael D

Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

2009 Volume 30, Issue 3, Page(s) 123–134

Abstract: The type III interferon (IFN) family elicits an antiviral response that is nearly identical to that evoked by IFN-alpha/beta. However, these cytokines (known as IFN-lambda1, 2, and 3) signal through a distinct receptor, and thus may be resistant to the ... ...

Abstract	The type III interferon (IFN) family elicits an antiviral response that is nearly identical to that evoked by IFN-alpha/beta. However, these cytokines (known as IFN-lambda1, 2, and 3) signal through a distinct receptor, and thus may be resistant to the evasion strategies used by some viruses to avoid the IFN-alpha/beta response. Orthopoxviruses are highly resistant to IFN-alpha/beta because they encode well-characterized immunomodulatory proteins that inhibit IFN activity. These include a secreted receptor (B18R) that neutralizes IFN-alpha/beta, and a cytoplasmic protein (E3L) that blocks IFN-alpha/beta effector functions in infected cells. We therefore determined the ability of these immunomodulators to abrogate the IFN-lambda-induced antiviral response. We found that (i) vaccinia virus (VACV) replication is resistant to IFN-lambda antiviral activity; (ii) neither VACV B18R nor the variola virus homolog B20R neutralizes IFN-lambda; (iii) VACV E3L inhibits the IFN-lambda-mediated antiviral response through a PKR-dependent pathway; (iv) VACV infection inhibits IFN-lambdaR-mediated signal transduction and gene expression. These results demonstrate differential sensitivity of IFN-lambda to multiple distinct evasion mechanisms employed by a single virus.
MeSH term(s)	Animals ; Cell Line, Tumor ; Cells, Cultured ; Gene Expression Regulation ; HeLa Cells ; Humans ; Immunologic Factors/genetics ; Immunologic Factors/metabolism ; Interferons/antagonists & inhibitors ; Interferons/genetics ; Interferons/pharmacology ; Mice ; RNA-Binding Proteins/metabolism ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/metabolism ; STAT Transcription Factors/metabolism ; Signal Transduction ; Vaccinia/physiopathology ; Vaccinia virus/drug effects ; Vaccinia virus/genetics ; Vaccinia virus/metabolism ; Vaccinia virus/physiology ; Variola virus/metabolism ; Vesiculovirus/metabolism ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Replication/drug effects
Chemical Substances	E3L protein, Vaccinia virus ; Immunologic Factors ; RNA-Binding Proteins ; STAT Transcription Factors ; Viral Proteins ; B18R protein, Vaccinia virus (135847-80-2) ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferons (9008-11-1)
Language	English
Publishing date	2009-12-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1226675-9
ISSN	1557-7465 ; 1079-9907
ISSN (online)	1557-7465
ISSN	1079-9907
DOI	10.1089/jir.2009.0049
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Article ; Online: Interferon-λ in HCV Infection and Therapy

Michael D. Robek / Nicole E. Pagliaccetti

Viruses, Vol 2, Iss 8, Pp 1589-

2010 Volume 1602

Abstract	Chronic infection with hepatitis C virus (HCV) is associated with significant liver disease and is therefore an important public health problem. The current standard-of-care therapy for chronic HCV infection consists of a combination of pegylated (PEG) interferon (IFN)-α and ribavirin. Although this therapy effectively generates a sustained viral response in approximately half of treated individuals, it is associated with significant hematological and neurological side effects. A new family of IFN-related proteins (IFN-λ1, 2, and 3; or alternately, IL-29, 28A, 28B, respectively) possesses properties that may make these cytokines superior to PEG-IFN-α for HCV therapy. Genetic studies have also implicated these proteins in both the natural and therapy-induced resolution of HCV infection. This review summarizes the basic aspects of IFN-λ biology, the potential role of these cytokines in HCV infection, and the outlook for their therapeutic application.
Keywords	IFN-λ ; IL-28 ; IL-29 ; type III interferon ; IL28B ; IL-28Rα ; Microbiology ; QR1-502 ; Science ; Q ; DOAJ:Microbiology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	570
Language	English
Publishing date	2010-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Lambda and alpha interferons inhibit hepatitis B virus replication through a common molecular mechanism but with different in vivo activities.

Pagliaccetti, Nicole E / Chu, Esther N / Bolen, Christopher R / Kleinstein, Steven H / Robek, Michael D

Virology

2010 Volume 401, Issue 2, Page(s) 197–206

Abstract: The type III interferons (IFN-lambda1, 2, and 3) induce an antiviral response similar to IFN-alpha/beta, but mediate their activity through a unique receptor. We found that like IFN-alpha/beta, IFN-lambda prevents the assembly of HBV capsids, ... ...

Abstract	The type III interferons (IFN-lambda1, 2, and 3) induce an antiviral response similar to IFN-alpha/beta, but mediate their activity through a unique receptor. We found that like IFN-alpha/beta, IFN-lambda prevents the assembly of HBV capsids, demonstrating convergence of the two signaling pathways through a single antiviral mechanism. In contrast to IFN-lambda, the structurally related cytokine interleukin (IL)-22 only minimally reduced HBV replication. The transcriptional program activated by IL-22 displayed little similarity to that induced by IFN-lambda, but instead resembled the response elicited by IL-6. We also found that murine IFN-lambda2 had only weak antiviral activity against HBV in the liver of transgenic mice, and that human IFN-lambda2 activity in serum correlated with the sensitivity of the cytokine to proteases. These results demonstrate that the IFN-alpha/beta and IFN-lambda anti-HBV responses operate through a single molecular mechanism, and support the notion that IFN-lambda plays a local, rather than systemic, role in antiviral immunity.
MeSH term(s)	Animals ; Cell Line ; Cells, Cultured ; Cytokines/immunology ; Gene Expression Profiling ; Hepatitis B virus/immunology ; Hepatitis B virus/physiology ; Hepatocytes/virology ; Humans ; Interferon-alpha/immunology ; Interleukins/immunology ; Mice ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; Virus Replication
Chemical Substances	Cytokines ; interferon-lambda, human ; Interferon-alpha ; Interleukins ; interferon-lambda protein, mouse
Language	English
Publishing date	2010-03-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2010.02.022
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Article: Interleukin-29 functions cooperatively with interferon to induce antiviral gene expression and inhibit hepatitis C virus replication.

Pagliaccetti, Nicole E / Eduardo, Roger / Kleinstein, Steven H / Mu, Xinmeng Jasmine / Bandi, Prasanthi / Robek, Michael D

The Journal of biological chemistry

2008 Volume 283, Issue 44, Page(s) 30079–30089

Abstract: The interferon (IFN)-related cytokine interleukin (IL)-29 (also known as IFN-lambda1) inhibits virus replication by inducing a cellular antiviral response similar to that activated by IFN-alpha/beta. However, because it binds to a unique receptor, this ... ...

Abstract	The interferon (IFN)-related cytokine interleukin (IL)-29 (also known as IFN-lambda1) inhibits virus replication by inducing a cellular antiviral response similar to that activated by IFN-alpha/beta. However, because it binds to a unique receptor, this cytokine may function cooperatively with IFN-alpha/beta or IFN-gamma during natural infections to inhibit virus replication, and might also be useful therapeutically in combination with other cytokines to treat chronic viral infections such as hepatitis C (HCV). We therefore investigated the ability of IL-29 and IFN-alpha or IFN-gamma to cooperatively inhibit virus replication and induce antiviral gene expression. Compared with the individual cytokines alone, the combination of IL-29 with IFN-alpha or IFN-gamma was more effective at blocking vesicular stomatitis virus and HCV replication, and this cooperative antiviral activity correlated with the magnitude of induced antiviral gene expression. Although the combined effects of IL-29 and IFN-alpha were primarily additive, the IL-29/IFN-gamma combination synergistically induced multiple genes and had the greatest antiviral activity. Two different mechanisms contributed to the enhanced gene expression induced by the cytokine combinations: increased activation of ISRE promoter elements and simultaneous activation of both ISRE and GAS elements within the same promoter. These findings provide new insight into the coregulation of a critical innate immune response by functionally distinct cytokine families.
MeSH term(s)	Antiviral Agents/pharmacology ; Base Sequence ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Gene Expression Profiling ; Gene Expression Regulation ; Hepacivirus/metabolism ; Hepatitis C/metabolism ; Hepatitis C/virology ; Humans ; Interferons/metabolism ; Interleukins/metabolism ; Models, Biological ; Molecular Sequence Data ; Promoter Regions, Genetic
Chemical Substances	Antiviral Agents ; interferon-lambda, human ; Interleukins ; Interferons (9008-11-1)
Language	English
Publishing date	2008-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M804296200
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Article: Interleukin-29 Functions Cooperatively with Interferon to Induce Antiviral Gene Expression and Inhibit Hepatitis C Virus Replication

Pagliaccetti, Nicole E / Eduardo, Roger / Kleinstein, Steven H / Mu, Xinmeng Jasmine / Bandi, Prasanthi / Robek, Michael D

Journal of biological chemistry. 2008 Oct. 31, v. 283, no. 44

2008

Abstract: The interferon (IFN)-related cytokine interleukin (IL)-29 (also known as IFN-λ1) inhibits virus replication by inducing a cellular antiviral response similar to that activated by IFN-α/β. However, because it binds to a unique receptor, this cytokine may ... ...

Abstract	The interferon (IFN)-related cytokine interleukin (IL)-29 (also known as IFN-λ1) inhibits virus replication by inducing a cellular antiviral response similar to that activated by IFN-α/β. However, because it binds to a unique receptor, this cytokine may function cooperatively with IFN-α/β or IFN-γ during natural infections to inhibit virus replication, and might also be useful therapeutically in combination with other cytokines to treat chronic viral infections such as hepatitis C (HCV). We therefore investigated the ability of IL-29 and IFN-α or IFN-γ to cooperatively inhibit virus replication and induce antiviral gene expression. Compared with the individual cytokines alone, the combination of IL-29 with IFN-α or IFN-γ was more effective at blocking vesicular stomatitis virus and HCV replication, and this cooperative antiviral activity correlated with the magnitude of induced antiviral gene expression. Although the combined effects of IL-29 and IFN-α were primarily additive, the IL-29/IFN-γ combination synergistically induced multiple genes and had the greatest antiviral activity. Two different mechanisms contributed to the enhanced gene expression induced by the cytokine combinations: increased activation of ISRE promoter elements and simultaneous activation of both ISRE and GAS elements within the same promoter. These findings provide new insight into the coregulation of a critical innate immune response by functionally distinct cytokine families.
Language	English
Dates of publication	2008-1031
Size	p. 30079-30089.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
Database	NAL-Catalogue (AGRICOLA)

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Article: Farnesol restores wild-type colony morphology to 96% of Candida albicans colony morphology variants recovered following treatment with mutagens.

Jensen, Ellen C / Hornby, Jacob M / Pagliaccetti, Nicole E / Wolter, Chuleeon M / Nickerson, Kenneth W / Atkin, Audrey L

Genome

2006 Volume 49, Issue 4, Page(s) 346–353

Abstract: Candida albicans is a diploid fungus that undergoes a morphological transition between budding yeast, hyphal, and pseudohyphal forms. The morphological transition is strongly correlated with virulence and is regulated in part by quorum sensing. Candida ... ...

Abstract	Candida albicans is a diploid fungus that undergoes a morphological transition between budding yeast, hyphal, and pseudohyphal forms. The morphological transition is strongly correlated with virulence and is regulated in part by quorum sensing. Candida albicans produces and secretes farnesol that regulates the yeast to mycelia morphological transition. Mutants that fail to synthesize or respond to farnesol could be locked in the filamentous mode. To test this hypothesis, a collection of C. albicans mutants were isolated that have altered colony morphologies indicative of the presence of hyphal cells under environmental conditions where C. albicans normally grows only as yeasts. All mutants were characterized for their ability to respond to farnesol. Of these, 95.9% fully or partially reverted to wild-type morphology on yeast malt (YM) agar plates supplemented with farnesol. All mutants that respond to farnesol regained their hyphal morphology when restreaked on YM plates without farnesol. The observation that farnesol remedial mutants are so common (95.9%) relative to mutants that fail to respond to farnesol (4.1%) suggests that farnesol activates and (or) induces a pathway that can override many of the morphogenesis defects in these mutants. Additionally, 9 mutants chosen at random were screened for farnesol production. Two mutants failed to produce detectable levels of farnesol.
MeSH term(s)	Candida albicans/growth & development ; Candida albicans/isolation & purification ; Candida albicans/physiology ; Ethyl Methanesulfonate/pharmacology ; Farnesol/metabolism ; Genetic Variation ; Hyphae/drug effects ; Hyphae/growth & development ; Mutagens/pharmacology ; Nitrous Acid/pharmacology ; Stem Cells/drug effects ; Ultraviolet Rays
Chemical Substances	Mutagens ; Farnesol (4602-84-0) ; Ethyl Methanesulfonate (9H154DI0UP) ; Nitrous Acid (T2I5UM75DN)
Language	English
Publishing date	2006-04
Publishing country	Canada
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639031-6
ISSN	1480-3321 ; 0831-2796
ISSN (online)	1480-3321
ISSN	0831-2796
DOI	10.1139/g05-117
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