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Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts

ABSTRACT: ISG20 is an interferon-regulated protein that exhibits RNase activity thereby inhibiting the replication of a broad spectrum of RNA viruses. By single cell RNA sequencing we identified ISG20 and several other interferon-regulated proteins as potential restriction factors against human cytomegalovirus (HCMV) since they were highly expressed in a cluster of HCMV resistant cells. Using an siRNA screening strategy we confirmed the antiviral action of ISG20.

ORGANISM(S): Homo sapiens

PROVIDER: GSE307708 | GEO | 2026/01/05

REPOSITORIES: GEO

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Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [SLAM-seq]

Project description:ISG20 is an interferon-regulated protein that exhibits Rnase activity thereby inhibiting the replication of a broad spectrum of RNA viruses. We identified ISG20 as a potential restriction factor against human cytomegalovirus (HCMV) that inhibits HCMV gene expression at the early stage of infection.In order to investigate whether ISG20 affects the half-life of cellular RNAs via its putative RNase activity, a SLAMseq experiment was performed. Interestingly, ISG20 expression resulted in an overall increased stablilty of cellular RNAs.

2026-01-05 | GSE307692 | GEO

Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [RNA-Seq]

Project description:ISG20 is an interferon-regulated protein that exhibits RNase activity thereby inhibiting the replication of a broad spectrum of RNA viruses. We identified ISG20 as a potential restriction factor against human cytomegalovirus (HCMV) that inhibits HCMV gene expression at the early stage of infection. However, neither the half-life of viral nor of cellular RNAs nor of viral DNA was decreased in ISG20-expressing cells. Instead, RNA-seq analysis revealed an innate immune defense signature upon ISG20 expression that comprised a distinct set of interferon-stimulated genes, zinc finger proteins and transposable elements.

2026-01-05 | GSE307691 | GEO

Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts

Project description:Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts

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Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [RNA-Seq]

Project description:Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [RNA-Seq]

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Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [SLAM-seq]

Project description:Interferon stimulated gene ISG20 induces an innate immune defense signature in primary human fibroblasts [SLAM-seq]

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Interferon-induced degradation of the hepatitis B virus persistence form, cccDNA, depends on ISG20

Project description:Hepatitis B virus (HBV) persists by depositing a covalently closed circular DNA (cccDNA) in the nucleus of infected cells that cannot be targeted by available antivirals. Cytokine treatments can diminish HBV cccDNA via APOBEC3-mediated deamination. Here we show that overexpression of APOBEC3A alone, however, was not sufficient to reduce cccDNA in HBV-infected cells. This required addition of interferon indicating that cccDNA degradation requires an additional, interferon-stimulated gene (ISG). Transcriptome analyses identified ISG20 as the only type I and II interferon-induced, nucleus-resident protein with annotated nuclease activity. ISG20 expression was detected in human livers in acute, self-limiting but not in chronic hepatitis B. ISG20 depletion abolished the interferon-induced loss of cccDNA, and co-expression of ISG20 and APOBEC3A was sufficient to diminish cccDNA. In conclusion, non-cytolytic HBV cccDNA decline requires induction of a deaminase and nuclease. Our findings highlight that ISGs cooperate for their antiviral function and this cooperativity may be explored for therapeutic targeting.

2021-04-22 | PXD019285 | Pride

Identification of ISG20 as the nuclease involved in interferon-induced decline of hepatitis B virus cccDNA

Project description:Hepatitis B virus (HBV) persists by depositing a covalently closed circular DNA (cccDNA) in the nucleus that cannot be targeted by available antivirals. Cytokine treatments can purge cccDNA from the nucleus of infected cells by APOBEC3-mediated deamination. cccDNA levels in HBV-infected cells were not reduced by overexpression of APOBEC3A alone, but only after simultaneous addition of interferon. This indicated the need of an additional, interferon-induced factor (ISG). Microarray analysis identified ISG20 as the only nuclease located to the nucleus induced by type I and II interferons. ISG20 was confirmed to be expressed in acute, self-limiting but not in chronic hepatitis B in human livers. ISG20 knockdown abolished the interferon-induced loss of cccDNA, and co-expression of ISG20 and APOBEC3A was sufficient to diminish cccDNA without further treatment. To conclude, nucleolar ISG20 was identified as the nuclease contributing to interferon-induced purging of HBV cccDNA, opening new avenues for antiviral targeting.

2020-07-22 | GSE134929 | GEO

Effect of ISG20 expression (wild-type or M1 mutant) on total RNA expression.

Project description:ISG20 is an interferon-induced 3'-to-5' RNA exonuclease that acts as a broad antiviral innate defense factor. At present, the features that expose RNA to the action of ISG20 remain unclear. However recent studies have pinpointed to RNA epitranscriptomic modifications as modulators that either expose or protect viral RNAs from ISG20, raising the question as to how cellular RNAs, on which these modifications are abundant, cope with ISG20. To obtain an unbiased perspective on this issue, we used RNAseq to pinpoint to the RNA elements that regulate the balance between susceptibility and resistance to ISG20.

2023-06-01 | GSE233792 | GEO

The interferon-induced exonuclease, ISG20, exerts antiviral activity through upregulation of type I interferon response proteins

Project description:Type I interferon-stimulated genes (ISGs) have critical roles in inhibiting virus replication and dissemination. Despite advances in understanding the molecular basis of ISG restriction, the antiviral mechanisms of many remain unclear. The 20 kDa ISG, ISG20, is a nuclear 3'-5'exonuclease with preference for single stranded RNA (ssRNA) and has been implicated in the IFN-mediated restriction of several RNA viruses. Although the exonuclease activity of ISG20 has been shown to degrade viral RNA in vitro, evidence has yet to be presented that virus inhibition in cells requires this activity. Here, we utilized a combination of an inducible, ectopic expression system and newly generated Isg20−/− mice to investigate mechanisms and consequences of ISG20-mediated restriction. Ectopically expressed ISG20 localized primarily to Cajal bodies in the nucleus and restricted replication of chikungunya and Venezuelan equine encephalitis viruses. Although restriction by ISG20 was associated with inhibition of translation of infecting genomic RNA, degradation of viral RNAs was not observed. Instead, translation inhibition of viral RNA was associated with ISG20-induced upregulation of over 100 other genes, many of which encode known antiviral effectors. ISG20 modulated the production of IFIT1, an ISG that suppresses translation of alphavirus RNAs. Consistent with this observation, the pathogenicity of IFIT1-sensitive alphaviruses was increased in Isg20−/− mice compared to wild-type viruses, but not in ISG20 ectopic-expressing cells. Our findings establish an indirect role for ISG20 in the early restriction of RNA virus replication by regulating expressionof other ISGs that inhibit translation and possibly other activities in the replication cycle.

2018-07-01 | GSE115729 | GEO

The interferon stimulated gene 20 protein (ISG20) is an innate defense antiviral factor that discriminates self versus non-self translation.

Project description:ISG20 is a broad spectrum antiviral protein thought to directly degrade viral RNA. However, this mechanism of inhibition remains controversial. Using the Vesicular Stomatitis Virus (VSV) as a model RNA virus, we show here that ISG20 interferes with viral replication by decreasing protein synthesis in the absence of RNA degradation. Importantly, we demonstrate that ISG20 exerts a translational control over a large panel of non-self RNA substrates including those originating from transfected DNA, while sparing endogenous transcripts. This activity correlates with the protein's ability to localize in cytoplasmic processing bodies. Finally, these functions are conserved in the ISG20 murine ortholog, whose genetic ablation results in mice with increased susceptibility to viral infection. Overall, our results posit ISG20 as an important defense factor able to discriminate the self/non-self origins of the RNA through translation modulation.

| S-EPMC6805002 | biostudies-literature

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