Single Nucleotide Polymorphisms in Genes for 2′‐5′‐Oligoadenylate Synthetase and RNase L in Patients Hospitalized with West Nile Virus Infection

Yakub, Imtiaz; Lillibridge, Kristy M.; Moran, Ana; González, Oscar; Belmont, John W.; Gibbs, Richard A.; Tweardy, David J.

doi:10.1086/497340

Cited by 120 publications

(90 citation statements)

References 32 publications

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“…Among them, one is a silent mutation located in the exon 2 at codon 136. In sequence comparison analysis using ESE Finder V3.0 (Cold Spring Harbor Laboratory) [26], the sequence surrounding this SNP was predicted to be a binding site for SF2/ASF splicing factor protein as reported by Yakub [25]. The sequence with the allele C matched with a 7-nt exonic splicing enhancer (ESE) consensus sequence, ctctCgt.…”

Section: Discussionmentioning

confidence: 74%

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Association of single nucleotide polymorphisms in interferon signaling pathway genes and interferon-stimulated genes with the response to interferon therapy for chronic hepatitis C

Yee

et al. 2008

Journal of Hepatology

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Section: Discussionmentioning

confidence: 74%

“…OAS is only activated by doublestranded RNA (dsRNA) while RNase L is activated by 2'-5'-oligoadenylate (2-5 A), which degrades dsRNA. OASL is postulated to interfere with the 2-5A system through blocking OAS activation [23][24][25]. Therefore, OASL may have a negative effect on anti-viral function of the OAS isozymes.…”

Section: Discussionmentioning

confidence: 99%

Association of single nucleotide polymorphisms in interferon signaling pathway genes and interferon-stimulated genes with the response to interferon therapy for chronic hepatitis C

Yee

et al. 2008

Journal of Hepatology

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“…So, for example, WNV interferes with pIC-induced activation of IRF3 (31), and the susceptibility of laboratory mice to WNV, as opposed to wild mice that are resistant, is linked to a polymorphism within the 2Ј5Јoligoadenylate synthetase (OAS) family of IFN-stimulated genes (ISG) (32). A similar occurrence of polymorphisms within the 2Ј5ЈOAS genes has been noted in patients hospitalized with WNV (33). The NS3/4A protein complex of hepatitis C virus also blocks phosphorylation of IRF3 (34).…”

Section: Discussionmentioning

confidence: 83%

TLR3 Ligation Activates an Antiviral Response in Human Fetal Astrocytes: A Role for Viperin/cig5

Rivieccio¹,

Suh²,

Zhao³

et al. 2006

The Journal of Immunology

129

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TLR3 functions as a viral nucleic acid sentinel activated by dsRNA viruses and virus replication intermediates within intracellular vesicles. To explore the spectrum of genes induced in human astrocytes by TLR3, we used a microarray approach and the analog polyriboinosinic polyribocytidylic acid (pIC) as ligand. As expected for TLR activation, pIC induced a wide array of cytokines and chemokines known for their role in inflammatory responses, as well as up-regulation of the receptor itself. The data also showed activation of a broad spectrum of antiviral response genes. To determine whether pIC induced an antiviral state in astrocytes, a pseudotyped HIV viral particle, vesicular stomatitis virus g-env-HIV-1, was used. pIC significantly abrogated HIV-1 replication, whereas IL-1, which also potently activates astrocytes, did not. One of the most highly up-regulated genes on microarray was the protein viperin/cig5. We found that viperin/cig5 expression was dependent on IFN regulatory factor 3 and NF-κB signaling, and that repetitive stimulation with pIC, but not IL-1, further increased expression. Viperin induction could also be substantially inhibited by neutralizing Abs to IFN-β, as could HIV-1 replication. To explore a role for viperin in IFN-β-mediated inhibition of HIV-1, we used an RNA interference (RNAi) approach. RNAi directed against viperin, but not a scrambled RNAi, significantly inhibited viperin expression, and also significantly reversed pIC-induced inhibition of HIV-1 replication. We conclude that viperin contributes to the antiviral state induced by TLR3 ligation in astrocytes, supporting a role for astrocytes as part of the innate immune response against infection in the CNS.

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“…ISGs (most importantly, PKR, OAS, and MxA) are the actual antiviral effectors. 44,45 It has been well demonstrated that the induction of type-I IFNs is required for activation of the IRF3/7 and NF-κB pathways. 46,47 IRF3, a constitutively expressed, phosphorylation-dependent regulatory factor, is activated by virus-induced phosphorylation, which leads to homodimerization, heterodimerization and nuclear translocation as well as its association with the co-activator CBP/p300.…”

Section: Discussionmentioning

confidence: 99%

Inducible Rubicon facilitates viral replication by antagonizing interferon production

et al. 2017

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The RUN domain Beclin-1-interacting cysteine-rich-containing (Rubicon) protein is involved in the maturation step of autophagy and the endocytic pathway as a Beclin-1-binding partner, but little is known regarding the role of Rubicon during viral infection. Here, we performed functional studies of the identified target in interferon (IFN) signaling pathways associated with Rubicon to elucidate the mechanisms of viral resistance to IFN. The Rubicon protein levels were elevated in peripheral blood mononuclear cells, sera and liver tissues from patients with hepatitis B virus (HBV) infection relative to those in healthy individuals. Assays of the overexpression and knockdown of Rubicon showed that Rubicon significantly promoted HBV replication. In addition, Rubicon knockdown resulted in the inhibition of enterovirus 71, influenza A virus and vesicular stomatitis virus. The expression o0f Rubicon led to the suppression of virus-induced type-I interferon (IFN-α and IFN-β) and type-III interferon (IFN-λ1). Translocation of activated IRF3 and IRF7 from the cytoplasm to the nucleus was involved in this process, and the NF-κB essential modulator (NEMO), a key factor in the IFN pathway, was the target with which Rubicon interacted. Our results reveal a previously unrecognized function of Rubicon as a virus-induced protein that binds to NEMO, leading to the inhibition of type-I interferon production. Rubicon thus functions as an important negative regulator of the innate immune response, enhances viral replication and may play a role in viral immune evasion.

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Single Nucleotide Polymorphisms in Genes for 2′‐5′‐Oligoadenylate Synthetase and RNase L in Patients Hospitalized with West Nile Virus Infection

Abstract: Because the reference allele contains a splice enhancer site, our finding suggests that the RNA transcripts generated from this allele may undergo increased splicing, which results in a dominant-negative OASL isozyme similar to the nonsense/truncation mutant form of Oas1b in mice.

Cited by 120 publications

References 32 publications

Association of single nucleotide polymorphisms in interferon signaling pathway genes and interferon-stimulated genes with the response to interferon therapy for chronic hepatitis C

Association of single nucleotide polymorphisms in interferon signaling pathway genes and interferon-stimulated genes with the response to interferon therapy for chronic hepatitis C

TLR3 Ligation Activates an Antiviral Response in Human Fetal Astrocytes: A Role for Viperin/cig5

Inducible Rubicon facilitates viral replication by antagonizing interferon production

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