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Article ; Online: Interferon-stimulated genes: new platforms and computational approaches.

Green, Richard / Ireton, Reneé C / Gale, Michael

Mammalian genome : official journal of the International Mammalian Genome Society

2018 Volume 29, Issue 7-8, Page(s) 593–602

Abstract: Interferon-stimulated genes (ISGs) are the effectors of interferon (IFN) actions and play major roles in innate immune defense against microbial infection. During virus infection, ISGs impart antiviral actions to control virus replication and spread but ... ...

Abstract	Interferon-stimulated genes (ISGs) are the effectors of interferon (IFN) actions and play major roles in innate immune defense against microbial infection. During virus infection, ISGs impart antiviral actions to control virus replication and spread but can also contribute to disease pathology if their expression is unchecked. Antiviral ISGs have been identified by a variety of biochemical, genetic, and virologic methods. New computational approaches are expanding and redefining ISGs as responders to a variety of stimuli beyond IFNs, including virus infection, stress, and other events that induce cytokines. These studies reveal that the expression of ISG subsets link to interferon regulatory factors (IRF)s, NF-kB, and other transcription factors that impart gene expression in specific cell types independently of IFNs, including stem cells and other cell types where ISGs are constitutively expressed. Here, we provide a broad overview of ISGs, define virus-induced genes (VSG)s, and discuss the application of computational approaches and bioinformatics platforms to evaluate the functional role of ISGs in epigenetics, immune programming, and vaccine responses.
MeSH term(s)	Animals ; Computational Biology/methods ; Gene Expression Regulation ; Genome-Wide Association Study/methods ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/genetics ; Interferons/metabolism ; Machine Learning ; Molecular Sequence Annotation ; Protein Binding ; Quantitative Trait Loci ; Response Elements ; Signal Transduction ; Vaccines/genetics ; Vaccines/immunology
Chemical Substances	Vaccines ; Interferons (9008-11-1)
Language	English
Publishing date	2018-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1058547-3
ISSN	1432-1777 ; 0938-8990
ISSN (online)	1432-1777
ISSN	0938-8990
DOI	10.1007/s00335-018-9755-6
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Article ; Online: Pushing to a cure by harnessing innate immunity against hepatitis C virus.

Ireton, Reneé C / Gale, Michael

Antiviral research

2014 Volume 108, Page(s) 156–164

Abstract: Hepatitis C virus (HCV) causes 350,000 deaths and infects at least 3million people worldwide every year. Currently no vaccine has been developed. Direct-acting antiviral (DAA) drugs with high efficacy for suppressing HCV infection have recently been ... ...

Abstract	Hepatitis C virus (HCV) causes 350,000 deaths and infects at least 3million people worldwide every year. Currently no vaccine has been developed. Direct-acting antiviral (DAA) drugs with high efficacy for suppressing HCV infection have recently been introduced into the clinic. While DAAs initially required combination therapy with type-1 interferon (IFN) administration for full efficacy and to avoid viral resistance to treatment, new DAA combinations show promise as an IFN-free regimen. However, IFN-free DAA therapy is in its infancy, still to be proven and today is cost-prohibitive for the patient. A major goal in HCV therapy to remove or replace IFN with DAAs or an alternative therapeutic to render virologic response with continued virus sensitivity to DAAs, thus facilitating a cure for infection. Recent advances in our understanding of innate immune responses to HCV have identified new therapeutic targets to combat HCV infection. We discuss how the targeting of innate immune response factors can be harnessed with DAAs to produce new generations of DAA-based HCV therapeutics. This article forms part of a symposium in Antiviral Research on "Hepatitis C: next steps toward global eradication."
MeSH term(s)	Antiviral Agents/therapeutic use ; Biomedical Research/trends ; Drug Discovery/trends ; Hepacivirus/drug effects ; Hepacivirus/immunology ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/immunology ; Humans ; Immunity, Innate ; Immunologic Factors/therapeutic use
Chemical Substances	Antiviral Agents ; Immunologic Factors
Language	English
Publishing date	2014-06-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2014.05.012
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Article ; Online: A Small Molecule RIG-I Agonist Serves as an Adjuvant to Induce Broad Multifaceted Influenza Virus Vaccine Immunity.

Hemann, Emily A / Knoll, Megan L / Wilkins, Courtney R / Subra, Caroline / Green, Richard / García-Sastre, Adolfo / Thomas, Paul G / Trautmann, Lydie / Ireton, Renee C / Loo, Yueh-Ming / Gale, Michael

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 210, Issue 9, Page(s) 1247–1256

Abstract: Retinoic acid-inducible gene I (RIG-I) is essential for activating host cell innate immunity to regulate the immune response against many RNA viruses. We previously identified that a small molecule compound, KIN1148, led to the activation of IFN ... ...

Abstract	Retinoic acid-inducible gene I (RIG-I) is essential for activating host cell innate immunity to regulate the immune response against many RNA viruses. We previously identified that a small molecule compound, KIN1148, led to the activation of IFN regulatory factor 3 (IRF3) and served to enhance protection against influenza A virus (IAV) A/California/04/2009 infection. We have now determined direct binding of KIN1148 to RIG-I to drive expression of IFN regulatory factor 3 and NF-κB target genes, including specific immunomodulatory cytokines and chemokines. Intriguingly, KIN1148 does not lead to ATPase activity or compete with ATP for binding but activates RIG-I to induce antiviral gene expression programs distinct from type I IFN treatment. When administered in combination with a vaccine against IAV, KIN1148 induces both neutralizing Ab and IAV-specific T cell responses compared with vaccination alone, which induces comparatively poor responses. This robust KIN1148-adjuvanted immune response protects mice from lethal A/California/04/2009 and H5N1 IAV challenge. Importantly, KIN1148 also augments human CD8+ T cell activation. Thus, we have identified a small molecule RIG-I agonist that serves as an effective adjuvant in inducing noncanonical RIG-I activation for induction of innate immune programs that enhance adaptive immune protection of antiviral vaccination.
MeSH term(s)	Humans ; Animals ; Mice ; Influenza Vaccines ; DEAD Box Protein 58/metabolism ; Influenza A Virus, H5N1 Subtype/metabolism ; Interferon Regulatory Factor-3/metabolism ; Adjuvants, Immunologic ; Influenza, Human ; Influenza A virus ; Antiviral Agents/pharmacology ; Immunity, Innate
Chemical Substances	Influenza Vaccines ; DEAD Box Protein 58 (EC 3.6.4.13) ; Interferon Regulatory Factor-3 ; Adjuvants, Immunologic ; Antiviral Agents
Language	English
Publishing date	2023-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300026
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Article ; Online: RNA PAMPs as Molecular Tools for Evaluating RIG-I Function in Innate Immunity.

Ireton, Renee C / Wilkins, Courtney / Gale, Michael

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1656, Page(s) 119–129

Abstract: Pathogen recognition receptors (PRR)s and their cognate pathogen-associated molecular pattern (PAMP) represent the basis of innate immune activation and immune response induction driven by the host-pathogen interaction that occurs during microbial ... ...

Abstract	Pathogen recognition receptors (PRR)s and their cognate pathogen-associated molecular pattern (PAMP) represent the basis of innate immune activation and immune response induction driven by the host-pathogen interaction that occurs during microbial infection in humans and other animals. For RNA virus infection such as hepatitis C virus (HCV) and others, specific motifs within viral RNA mark it as nonself and visible to the host as a PAMP through interaction with RIG-I-like receptors including retinoic inducible gene-I (RIG-I). Here, we present methods for producing and using HCV PAMP RNA as a molecular tool to study RIG-I and its signaling pathway, both in vitro and in vivo, in innate immune regulation.
MeSH term(s)	Animals ; Cell Line ; DEAD Box Protein 58/genetics ; DEAD Box Protein 58/immunology ; Hepacivirus/genetics ; Hepacivirus/immunology ; Hepatitis C/genetics ; Hepatitis C/immunology ; Humans ; Immunity, Innate ; RNA, Viral/chemistry ; RNA, Viral/genetics ; RNA, Viral/immunology ; Receptors, Immunologic ; Receptors, Pattern Recognition/genetics ; Receptors, Pattern Recognition/immunology
Chemical Substances	RNA, Viral ; Receptors, Immunologic ; Receptors, Pattern Recognition ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13)
Language	English
Publishing date	2017-08-14
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7237-1_6
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Article ; Online: Viral Resistance Analyses From the Remdesivir Phase 3 Adaptive COVID-19 Treatment Trial-1 (ACTT-1).

Hedskog, Charlotte / Rodriguez, Lauren / Roychoudhury, Pavitra / Huang, Meei-Li / Jerome, Keith R / Hao, Linhui / Ireton, Renee C / Li, Jiani / Perry, Jason K / Han, Dong / Camus, Gregory / Greninger, Alexander L / Gale, Michael / Porter, Danielle P

The Journal of infectious diseases

2023 Volume 228, Issue 9, Page(s) 1263–1273

Abstract: Background: Remdesivir is approved for treatment of coronavirus disease 2019 (COVID-19) in nonhospitalized and hospitalized adult and pediatric patients. Here we present severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resistance analyses ... ...

Abstract	Background: Remdesivir is approved for treatment of coronavirus disease 2019 (COVID-19) in nonhospitalized and hospitalized adult and pediatric patients. Here we present severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resistance analyses from the phase 3 ACTT-1 randomized placebo-controlled trial conducted in adult participants hospitalized with COVID-19. Methods: Swab samples were collected at baseline and longitudinally through day 29. SARS-CoV-2 genomes were sequenced using next-generation sequencing. Phenotypic analysis was conducted directly on participant virus isolates and/or using SARS-CoV-2 subgenomic replicons expressing mutations identified in the Nsp12 target gene. Results: Among participants with both baseline and postbaseline sequencing data, emergent Nsp12 substitutions were observed in 12 of 31 (38.7%) and 12 of 30 (40.0%) participants in the remdesivir and placebo arms, respectively. No emergent Nsp12 substitutions in the remdesivir arm were observed in more than 1 participant. Phenotyping showed low to no change in susceptibility to remdesivir relative to wild-type Nsp12 reference for the substitutions tested: A16V (0.8-fold change in EC50), P323L + V792I (2.2-fold), C799F (2.5-fold), K59N (1.0-fold), and K59N + V792I (3.4-fold). Conclusions: The similar rate of emerging Nsp12 substitutions in the remdesivir and placebo arms and the minimal change in remdesivir susceptibility among tested substitutions support a high barrier to remdesivir resistance development in COVID-19 patients. Clinical Trials Registration. NCT04280705.
MeSH term(s)	Adult ; Humans ; Child ; COVID-19 ; SARS-CoV-2/genetics ; COVID-19 Drug Treatment ; Adenosine Monophosphate/therapeutic use ; Alanine/therapeutic use ; Antiviral Agents/therapeutic use
Chemical Substances	remdesivir (3QKI37EEHE) ; Adenosine Monophosphate (415SHH325A) ; Alanine (OF5P57N2ZX) ; Antiviral Agents
Language	English
Publishing date	2023-07-19
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase III ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiad270
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Article: Systems biology analyses to define host responses to HCV infection and therapy.

Ireton, Reneé C / Gale, Michael

Current topics in microbiology and immunology

2013 Volume 363, Page(s) 143–167

Abstract: While 170 million people worldwide are chronically infected with HCV, the response rate to the current treatment regimens of pegylated IFN-α (IFN) in combination with ribavirin is only approximately 55 % of all HCV patients undergoing therapy. This IFN- ... ...

Abstract	While 170 million people worldwide are chronically infected with HCV, the response rate to the current treatment regimens of pegylated IFN-α (IFN) in combination with ribavirin is only approximately 55 % of all HCV patients undergoing therapy. This IFN-based therapy is now slated to serve as the backbone for future combination therapeutics involving direct-acting antiviral compounds, including HCV protease inhibitors, viral polymerase inhibitors, and other small molecules. It is essential that the application of IFN be improved for overall enhancement of therapy outcome to effectively cure HCV infection. Systems approaches, including genomics and network modeling, are particularly powerful tools that are now being used to dissect the underlying mechanisms of successful or failed treatment response in an effort to design improved IFN-based therapeutic regimens. Furthermore, systems applications can be used to define virus-host interactions and map their variation within viral and host genomes, leading to identification of targets for novel therapy strategies. Using these approaches, we have defined distinct hepatic expression and tissue distribution of innate immune signaling molecules and gene networks that associate with IFN-based treatment outcome for HCV infection. This chapter will focus on using systems approaches to understand the host response to both HCV infection and therapy to drive the development of improved HCV therapeutics.
MeSH term(s)	Animals ; Hepatitis C/drug therapy ; Hepatitis C/immunology ; Humans ; Immune Evasion ; Systems Biology/methods ; Treatment Outcome
Language	English
Publishing date	2013
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/82_2012_251
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Article ; Online: RIG-I like receptors in antiviral immunity and therapeutic applications.

Ireton, Reneé C / Gale, Michael

Viruses

2011 Volume 3, Issue 6, Page(s) 906–919

Abstract: The RNA helicase family of RIG-I-like receptors (RLRs) is a key component of host defense mechanisms responsible for detecting viruses and triggering innate immune signaling cascades to control viral replication and dissemination. As cytoplasm-based ... ...

Abstract	The RNA helicase family of RIG-I-like receptors (RLRs) is a key component of host defense mechanisms responsible for detecting viruses and triggering innate immune signaling cascades to control viral replication and dissemination. As cytoplasm-based sensors, RLRs recognize foreign RNA in the cell and activate a cascade of antiviral responses including the induction of type I interferons, inflammasome activation, and expression of proinflammatory cytokines and chemokines. This review provides a brief overview of RLR function, ligand interactions, and downstream signaling events with an expanded discussion on the therapeutic potential of targeting RLRs for immune stimulation and treatment of virus infection.
MeSH term(s)	Animals ; Antiviral Agents/therapeutic use ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/immunology ; Enzyme Activators/therapeutic use ; Humans ; Immunity, Innate ; Virus Diseases/drug therapy ; Virus Diseases/enzymology ; Virus Diseases/immunology ; Virus Diseases/virology ; Virus Physiological Phenomena ; Viruses/drug effects
Chemical Substances	Antiviral Agents ; Enzyme Activators ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2011-06-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v3060906
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Article: EphA2 receptor tyrosine kinase as a promising target for cancer therapeutics.

Ireton, Reneé C / Chen, Jin

Current cancer drug targets

2005 Volume 5, Issue 3, Page(s) 149–157

Abstract: Eph receptors are a unique family of receptor tyrosine kinases (RTK) that play critical roles in embryonic patterning, neuronal targeting, and vascular development during normal embryogenesis. Eph RTKs and their ligands, the ephrins, are also frequently ... ...

Abstract	Eph receptors are a unique family of receptor tyrosine kinases (RTK) that play critical roles in embryonic patterning, neuronal targeting, and vascular development during normal embryogenesis. Eph RTKs and their ligands, the ephrins, are also frequently overexpressed in a variety of cancers and tumor cell lines. In particular, one family member, EphA2, is overexpressed in breast, prostate, lung, and colon cancers. Unlike traditional oncogenes that often function only in tumor cells, recent data show that Eph receptors mediate cell-cell interactions both in tumor cells and in the tumor microenvironment, namely the tumor stroma and tumor vasculature. Thus, EphA2 receptors are attractive targets for drug design, as targeting these molecules could simultaneously inhibit several aspects of tumor progression. This review focuses on the multiple roles of EphA2 in cancer progression, the mechanisms by which EphA2 inhibition may halt this progression, and the pre-clinical results of EphA2 inhibition in various cancer model systems.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Receptor, EphA2/biosynthesis ; Receptor, EphA2/drug effects
Chemical Substances	Antineoplastic Agents ; Receptor, EphA2 (EC 2.7.10.1)
Language	English
Publishing date	2005-03-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	2064824-8
ISSN	1873-5576 ; 1568-0096
ISSN (online)	1873-5576
ISSN	1568-0096
DOI	10.2174/1568009053765780
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Zs.A 5589: Show issues

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Article ; Online: Duration of viral infectiousness and correlation with symptoms and diagnostic testing in non-hospitalized adults during acute SARS-CoV-2 infection: A longitudinal cohort study.

Drain, Paul K / Dalmat, Ronit R / Hao, Linhui / Bemer, Meagan J / Budiawan, Elvira / Morton, Jennifer F / Ireton, Renee C / Hsiang, Tien-Ying / Marfatia, Zarna / Prabhu, Roshni / Woosley, Claire / Gichamo, Adanech / Rechkina, Elena / Hamilton, Daphne / Montaño, Michalina / Cantera, Jason L / Ball, Alexey S / Golez, Inah / Smith, Elise /

Greninger, Alexander L / McElrath, M Juliana / Thompson, Matthew / Grant, Benjamin D / Meisner, Allison / Gottlieb, Geoffrey S / Gale, Michael

Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology

2023 Volume 161, Page(s) 105420

Abstract: Background: Guidelines for SARS-CoV-2 have relied on limited data on duration of viral infectiousness and correlation with COVID-19 symptoms and diagnostic testing.: Methods: We enrolled ambulatory adults with acute SARS-CoV-2 infection and performed ...

Abstract	Background: Guidelines for SARS-CoV-2 have relied on limited data on duration of viral infectiousness and correlation with COVID-19 symptoms and diagnostic testing. Methods: We enrolled ambulatory adults with acute SARS-CoV-2 infection and performed serial measurements of COVID-19 symptoms, nasal swab viral RNA, nucleocapsid (N) and spike (S) antigens, and replication-competent SARS-CoV-2 by viral growth in culture. We determined average time from symptom onset to a first negative test result and estimated risk of infectiousness, as defined by positive viral growth in culture. Results: Among 95 adults, median [interquartile range] time from symptom onset to first negative test result was 9 [5] days, 13 [6] days, 11 [4] days, and >19 days for S antigen, N antigen, culture growth, and viral RNA by RT-PCR, respectively. Beyond two weeks, virus growth and N antigen titers were rarely positive, while viral RNA remained detectable among half (26/51) of participants tested 21-30 days after symptom onset. Between 6-10 days from symptom onset, N antigen was strongly associated with culture positivity (relative risk=7.61, 95% CI: 3.01-19.22), whereas neither viral RNA nor symptoms were associated with culture positivity. During the 14 days following symptom onset, the presence of N antigen remained strongly associated (adjusted relative risk=7.66, 95% CI: 3.96-14.82) with culture positivity, regardless of COVID-19 symptoms. Conclusions: Most adults have replication-competent SARS-CoV-2 for 10-14 after symptom onset. N antigen testing is a strong predictor of viral infectiousness and may be a more suitable biomarker, rather than absence of symptoms or viral RNA, to discontinue isolation within two weeks from symptom onset.
MeSH term(s)	Adult ; Humans ; COVID-19/diagnosis ; SARS-CoV-2 ; Longitudinal Studies ; Diagnostic Techniques and Procedures ; RNA, Viral ; COVID-19 Testing
Chemical Substances	RNA, Viral
Language	English
Publishing date	2023-03-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1446080-4
ISSN	1873-5967 ; 1386-6532
ISSN (online)	1873-5967
ISSN	1386-6532
DOI	10.1016/j.jcv.2023.105420
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Article ; Online: Immune Correlates of Protection From West Nile Virus Neuroinvasion and Disease.

Graham, Jessica B / Swarts, Jessica L / Thomas, Sunil / Voss, Kathleen M / Sekine, Aimee / Green, Richard / Ireton, Renee C / Gale, Michael / Lund, Jennifer M

The Journal of infectious diseases

2018 Volume 219, Issue 7, Page(s) 1162–1171

Abstract: Background: A challenge to the design of improved therapeutic agents and prevention strategies for neuroinvasive infection and associated disease is the lack of known natural immune correlates of protection. A relevant model to study such correlates is ... ...

Abstract	Background: A challenge to the design of improved therapeutic agents and prevention strategies for neuroinvasive infection and associated disease is the lack of known natural immune correlates of protection. A relevant model to study such correlates is offered by the Collaborative Cross (CC), a panel of recombinant inbred mouse strains that exhibit a range of disease manifestations upon infection. Methods: We performed an extensive screen of CC-F1 lines infected with West Nile virus (WNV), including comprehensive immunophenotyping, to identify groups of lines that exhibited viral neuroinvasion or neuroinvasion with disease and lines that remained free of WNV neuroinvasion and disease. Results: Our data reveal that protection from neuroinvasion and disease is multifactorial and that several immune outcomes can contribute. Immune correlates identified include decreased suppressive activity of regulatory T cells at steady state, which correlates with peripheral restriction of the virus. Further, a rapid contraction of WNV-specific CD8+ T cells in the brain correlated with protection from disease. Conclusions: These immune correlates of protection illustrate additional networks and pathways of the WNV immune response that cannot be observed in the C57BL/6 mouse model. Additionally, correlates of protection exhibited before infection, at baseline, provide insight into phenotypic differences in the human population that may predict clinical outcomes upon infection.
MeSH term(s)	2',5'-Oligoadenylate Synthetase/genetics ; Adaptive Immunity ; Animals ; Brain/immunology ; Brain/pathology ; CD4-CD8 Ratio ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Collaborative Cross Mice/genetics ; Collaborative Cross Mice/immunology ; Disease Models, Animal ; Heterozygote ; Immunity, Innate ; Immunophenotyping ; Male ; Mice ; Mice, Inbred C57BL ; Nervous System Diseases/immunology ; Nervous System Diseases/microbiology ; Polymorphism, Genetic ; Spleen/immunology ; Spleen/pathology ; T-Lymphocytes, Regulatory/immunology ; West Nile Fever/complications ; West Nile Fever/genetics ; West Nile Fever/immunology ; West Nile virus/immunology
Chemical Substances	Oas1b protein, mouse (EC 2.7.7.-) ; 2',5'-Oligoadenylate Synthetase (EC 2.7.7.84)
Language	English
Publishing date	2018-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiy623
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